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ESP: PubMed Auto Bibliography 26 Sep 2023 at 01:46 Created:
Evolution of Multicelluarity
Created with PubMed® Query: ( (evolution OR origin) AND (multicellularity OR multicellular) NOT 33634751[PMID] ) NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2023-09-25
Physiological potential and evolutionary trajectories of syntrophic sulfate-reducing bacterial partners of anaerobic methanotrophic archaea.
PLoS biology, 21(9):e3002292 pii:PBIOLOGY-D-22-02613 [Epub ahead of print].
Sulfate-coupled anaerobic oxidation of methane (AOM) is performed by multicellular consortia of anaerobic methanotrophic (ANME) archaea in obligate syntrophic partnership with sulfate-reducing bacteria (SRB). Diverse ANME and SRB clades co-associate but the physiological basis for their adaptation and diversification is not well understood. In this work, we used comparative metagenomics and phylogenetics to investigate the metabolic adaptation among the 4 main syntrophic SRB clades (HotSeep-1, Seep-SRB2, Seep-SRB1a, and Seep-SRB1g) and identified features associated with their syntrophic lifestyle that distinguish them from their non-syntrophic evolutionary neighbors in the phylum Desulfobacterota. We show that the protein complexes involved in direct interspecies electron transfer (DIET) from ANME to the SRB outer membrane are conserved between the syntrophic lineages. In contrast, the proteins involved in electron transfer within the SRB inner membrane differ between clades, indicative of convergent evolution in the adaptation to a syntrophic lifestyle. Our analysis suggests that in most cases, this adaptation likely occurred after the acquisition of the DIET complexes in an ancestral clade and involve horizontal gene transfers within pathways for electron transfer (CbcBA) and biofilm formation (Pel). We also provide evidence for unique adaptations within syntrophic SRB clades, which vary depending on the archaeal partner. Among the most widespread syntrophic SRB, Seep-SRB1a, subclades that specifically partner ANME-2a are missing the cobalamin synthesis pathway, suggestive of nutritional dependency on its partner, while closely related Seep-SRB1a partners of ANME-2c lack nutritional auxotrophies. Our work provides insight into the features associated with DIET-based syntrophy and the adaptation of SRB towards it.
Additional Links: PMID-37747940
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@article {pmid37747940,
year = {2023},
author = {Murali, R and Yu, H and Speth, DR and Wu, F and Metcalfe, KS and Crémière, A and Laso-Pèrez, R and Malmstrom, RR and Goudeau, D and Woyke, T and Hatzenpichler, R and Chadwick, GL and Connon, SA and Orphan, VJ},
title = {Physiological potential and evolutionary trajectories of syntrophic sulfate-reducing bacterial partners of anaerobic methanotrophic archaea.},
journal = {PLoS biology},
volume = {21},
number = {9},
pages = {e3002292},
doi = {10.1371/journal.pbio.3002292},
pmid = {37747940},
issn = {1545-7885},
abstract = {Sulfate-coupled anaerobic oxidation of methane (AOM) is performed by multicellular consortia of anaerobic methanotrophic (ANME) archaea in obligate syntrophic partnership with sulfate-reducing bacteria (SRB). Diverse ANME and SRB clades co-associate but the physiological basis for their adaptation and diversification is not well understood. In this work, we used comparative metagenomics and phylogenetics to investigate the metabolic adaptation among the 4 main syntrophic SRB clades (HotSeep-1, Seep-SRB2, Seep-SRB1a, and Seep-SRB1g) and identified features associated with their syntrophic lifestyle that distinguish them from their non-syntrophic evolutionary neighbors in the phylum Desulfobacterota. We show that the protein complexes involved in direct interspecies electron transfer (DIET) from ANME to the SRB outer membrane are conserved between the syntrophic lineages. In contrast, the proteins involved in electron transfer within the SRB inner membrane differ between clades, indicative of convergent evolution in the adaptation to a syntrophic lifestyle. Our analysis suggests that in most cases, this adaptation likely occurred after the acquisition of the DIET complexes in an ancestral clade and involve horizontal gene transfers within pathways for electron transfer (CbcBA) and biofilm formation (Pel). We also provide evidence for unique adaptations within syntrophic SRB clades, which vary depending on the archaeal partner. Among the most widespread syntrophic SRB, Seep-SRB1a, subclades that specifically partner ANME-2a are missing the cobalamin synthesis pathway, suggestive of nutritional dependency on its partner, while closely related Seep-SRB1a partners of ANME-2c lack nutritional auxotrophies. Our work provides insight into the features associated with DIET-based syntrophy and the adaptation of SRB towards it.},
}
RevDate: 2023-09-24
Origin, evolution, and diversification of the wall-associated kinase gene family in plants.
Plant cell reports [Epub ahead of print].
The study of the origin, evolution, and diversification of the wall-associated kinase gene family in plants facilitates their functional investigations in the future. Wall-associated kinases (WAKs) make up one subfamily of receptor-like kinases (RLKs), and function directly in plant cell elongation and responses to biotic and abiotic stresses. The biological functions of WAKs have been extensively characterized in angiosperms; however, the origin and evolutionary history of the WAK family in green plants remain unclear. Here, we performed a comprehensive analysis of the WAK family to reveal its origin, evolution, and diversification in green plants. In total, 1061 WAK genes were identified in 37 species from unicellular algae to multicellular plants, and the results showed that WAK genes probably originated before bryophyte differentiation and were widely distributed in land plants, especially angiosperms. The phylogeny indicated that the land plant WAKs gave rise to five clades and underwent lineage-specific expansion after species differentiation. Cis-acting elements and expression patterns analyses of WAK genes in Arabidopsis and rice demonstrated the functional diversity of WAK genes in these two species. Many gene gains and losses have occurred in angiosperms, leading to an increase in the number of gene copies. The evolutionary trajectory of the WAK family during polyploidization was uncovered using Gossypium species. Our results provide insights into the evolution of WAK genes in green plants, facilitating their functional investigations in the future.
Additional Links: PMID-37743376
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@article {pmid37743376,
year = {2023},
author = {Zhang, Z and Huo, W and Wang, X and Ren, Z and Zhao, J and Liu, Y and He, K and Zhang, F and Li, W and Jin, S and Yang, D},
title = {Origin, evolution, and diversification of the wall-associated kinase gene family in plants.},
journal = {Plant cell reports},
volume = {},
number = {},
pages = {},
pmid = {37743376},
issn = {1432-203X},
support = {232300421116//Natural Science Foundation of Henan Province/ ; },
abstract = {The study of the origin, evolution, and diversification of the wall-associated kinase gene family in plants facilitates their functional investigations in the future. Wall-associated kinases (WAKs) make up one subfamily of receptor-like kinases (RLKs), and function directly in plant cell elongation and responses to biotic and abiotic stresses. The biological functions of WAKs have been extensively characterized in angiosperms; however, the origin and evolutionary history of the WAK family in green plants remain unclear. Here, we performed a comprehensive analysis of the WAK family to reveal its origin, evolution, and diversification in green plants. In total, 1061 WAK genes were identified in 37 species from unicellular algae to multicellular plants, and the results showed that WAK genes probably originated before bryophyte differentiation and were widely distributed in land plants, especially angiosperms. The phylogeny indicated that the land plant WAKs gave rise to five clades and underwent lineage-specific expansion after species differentiation. Cis-acting elements and expression patterns analyses of WAK genes in Arabidopsis and rice demonstrated the functional diversity of WAK genes in these two species. Many gene gains and losses have occurred in angiosperms, leading to an increase in the number of gene copies. The evolutionary trajectory of the WAK family during polyploidization was uncovered using Gossypium species. Our results provide insights into the evolution of WAK genes in green plants, facilitating their functional investigations in the future.},
}
RevDate: 2023-09-23
Course-, dose-, and stage-dependent toxic effects of prenatal acetaminophen exposure on fetal long bone development.
Toxicology letters pii:S0378-4274(23)01045-7 [Epub ahead of print].
Acetaminophen is a common analgesic and fever reduction medicine for pregnant women. Epidemiological studies suggest that prenatal acetaminophen usage affects offspring health and development. However, the effects of prenatal acetaminophen exposure (PAcE) on fetal long bone development and its potential mechanisms have not been elucidated. Based on clinical dosing characteristics, fetal mouse femurs were obtained for detection after oral gavage of acetaminophen at different doses (0, 100 or 400mg/kg d), courses (single or multiple times) or stages (mid- or late pregnancy) during pregnancy in Kunming mice. The results showed that compared with the control group, PAcE reduced the length of total femur and the primary ossification center (POC), delayed the mineralization of POC and the ossification of epiphyseal region, and down-regulated the mRNA expression of osteogenic function markers (such as Runx2, Bsp, Ocn, Col1a1) in fetal femur, particularly in the high dose, multiple courses, and mid-pregnancy group. Meanwhile, the osteoclast and angiogenic function were also inhibited by PAcE at high dose, multiple courses, and mid-pregnancy, but the inhibition level was less than osteogenic function. Moreover, the alteration of canonical Wnt signalling pathway in PAcE fetal bone were consistent with its osteogenesis function changes. In conclusion, PAcE caused development toxicity and multi-cellular function inhibition in fetal long bone, particularly in the high dose, multiple treatments and mid-pregnancy group, and the alteration of canonical Wnt signalling pathway may be its potential mechanism.
Additional Links: PMID-37741353
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@article {pmid37741353,
year = {2023},
author = {Ma, C and Li, X and Xiao, H and Li, B and Gu, H and Guo, Y and Wang, H and Wen, Y and Chen, L},
title = {Course-, dose-, and stage-dependent toxic effects of prenatal acetaminophen exposure on fetal long bone development.},
journal = {Toxicology letters},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.toxlet.2023.09.007},
pmid = {37741353},
issn = {1879-3169},
abstract = {Acetaminophen is a common analgesic and fever reduction medicine for pregnant women. Epidemiological studies suggest that prenatal acetaminophen usage affects offspring health and development. However, the effects of prenatal acetaminophen exposure (PAcE) on fetal long bone development and its potential mechanisms have not been elucidated. Based on clinical dosing characteristics, fetal mouse femurs were obtained for detection after oral gavage of acetaminophen at different doses (0, 100 or 400mg/kg d), courses (single or multiple times) or stages (mid- or late pregnancy) during pregnancy in Kunming mice. The results showed that compared with the control group, PAcE reduced the length of total femur and the primary ossification center (POC), delayed the mineralization of POC and the ossification of epiphyseal region, and down-regulated the mRNA expression of osteogenic function markers (such as Runx2, Bsp, Ocn, Col1a1) in fetal femur, particularly in the high dose, multiple courses, and mid-pregnancy group. Meanwhile, the osteoclast and angiogenic function were also inhibited by PAcE at high dose, multiple courses, and mid-pregnancy, but the inhibition level was less than osteogenic function. Moreover, the alteration of canonical Wnt signalling pathway in PAcE fetal bone were consistent with its osteogenesis function changes. In conclusion, PAcE caused development toxicity and multi-cellular function inhibition in fetal long bone, particularly in the high dose, multiple treatments and mid-pregnancy group, and the alteration of canonical Wnt signalling pathway may be its potential mechanism.},
}
RevDate: 2023-09-20
The origin of eukaryotes and rise in complexity were synchronous with the rise in oxygen.
Frontiers in bioinformatics, 3:1233281.
The origin of eukaryotes was among the most important events in the history of life, spawning a new evolutionary lineage that led to all complex multicellular organisms. However, the timing of this event, crucial for understanding its environmental context, has been difficult to establish. The fossil and biomarker records are sparse and molecular clocks have thus far not reached a consensus, with dates spanning 2.1-0.91 billion years ago (Ga) for critical nodes. Notably, molecular time estimates for the last common ancestor of eukaryotes are typically hundreds of millions of years younger than the Great Oxidation Event (GOE, 2.43-2.22 Ga), leading researchers to question the presumptive link between eukaryotes and oxygen. We obtained a new time estimate for the origin of eukaryotes using genetic data of both archaeal and bacterial origin, the latter rarely used in past studies. We also avoided potential calibration biases that may have affected earlier studies. We obtained a conservative interval of 2.2-1.5 Ga, with an even narrower core interval of 2.0-1.8 Ga, for the origin of eukaryotes, a period closely aligned with the rise in oxygen. We further reconstructed the history of biological complexity across the tree of life using three universal measures: cell types, genes, and genome size. We found that the rise in complexity was temporally consistent with and followed a pattern similar to the rise in oxygen. This suggests a causal relationship stemming from the increased energy needs of complex life fulfilled by oxygen.
Additional Links: PMID-37727796
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@article {pmid37727796,
year = {2023},
author = {Craig, JM and Kumar, S and Hedges, SB},
title = {The origin of eukaryotes and rise in complexity were synchronous with the rise in oxygen.},
journal = {Frontiers in bioinformatics},
volume = {3},
number = {},
pages = {1233281},
pmid = {37727796},
issn = {2673-7647},
abstract = {The origin of eukaryotes was among the most important events in the history of life, spawning a new evolutionary lineage that led to all complex multicellular organisms. However, the timing of this event, crucial for understanding its environmental context, has been difficult to establish. The fossil and biomarker records are sparse and molecular clocks have thus far not reached a consensus, with dates spanning 2.1-0.91 billion years ago (Ga) for critical nodes. Notably, molecular time estimates for the last common ancestor of eukaryotes are typically hundreds of millions of years younger than the Great Oxidation Event (GOE, 2.43-2.22 Ga), leading researchers to question the presumptive link between eukaryotes and oxygen. We obtained a new time estimate for the origin of eukaryotes using genetic data of both archaeal and bacterial origin, the latter rarely used in past studies. We also avoided potential calibration biases that may have affected earlier studies. We obtained a conservative interval of 2.2-1.5 Ga, with an even narrower core interval of 2.0-1.8 Ga, for the origin of eukaryotes, a period closely aligned with the rise in oxygen. We further reconstructed the history of biological complexity across the tree of life using three universal measures: cell types, genes, and genome size. We found that the rise in complexity was temporally consistent with and followed a pattern similar to the rise in oxygen. This suggests a causal relationship stemming from the increased energy needs of complex life fulfilled by oxygen.},
}
RevDate: 2023-09-20
Multispecies interactions shape the transition to multicellularity.
Proceedings. Biological sciences, 290(2007):20231055.
The origin of multicellularity transformed the adaptive landscape on Earth, opening diverse avenues for further innovation. The transition to multicellular life is understood as the evolution of cooperative groups which form a new level of individuality. Despite the potential for community-level interactions, most studies have not addressed the competitive context of this transition, such as competition between species. Here, we explore how interspecific competition shapes the emergence of multicellularity in an experimental system with two yeast species, Saccharomyces cerevisiae and Kluyveromyces lactis, where multicellularity evolves in response to selection for faster settling ability. We find that the multispecies context slows the rate of the transition to multicellularity, and the transition to multicellularity significantly impacts community composition. Multicellular K. lactis emerges first and sweeps through populations in monocultures faster than in cocultures with S. cerevisiae. Following the transition, the between-species competitive dynamics shift, likely in part to intraspecific cooperation in K. lactis. Hence, we document an eco-evolutionary feedback across the transition to multicellularity, underscoring how ecological context is critical for understanding the causes and consequences of innovation. By including two species, we demonstrate that cooperation and competition across several biological scales shapes the origin and persistence of multicellularity.
Additional Links: PMID-37727086
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@article {pmid37727086,
year = {2023},
author = {Kalambokidis, M and Travisano, M},
title = {Multispecies interactions shape the transition to multicellularity.},
journal = {Proceedings. Biological sciences},
volume = {290},
number = {2007},
pages = {20231055},
doi = {10.1098/rspb.2023.1055},
pmid = {37727086},
issn = {1471-2954},
abstract = {The origin of multicellularity transformed the adaptive landscape on Earth, opening diverse avenues for further innovation. The transition to multicellular life is understood as the evolution of cooperative groups which form a new level of individuality. Despite the potential for community-level interactions, most studies have not addressed the competitive context of this transition, such as competition between species. Here, we explore how interspecific competition shapes the emergence of multicellularity in an experimental system with two yeast species, Saccharomyces cerevisiae and Kluyveromyces lactis, where multicellularity evolves in response to selection for faster settling ability. We find that the multispecies context slows the rate of the transition to multicellularity, and the transition to multicellularity significantly impacts community composition. Multicellular K. lactis emerges first and sweeps through populations in monocultures faster than in cocultures with S. cerevisiae. Following the transition, the between-species competitive dynamics shift, likely in part to intraspecific cooperation in K. lactis. Hence, we document an eco-evolutionary feedback across the transition to multicellularity, underscoring how ecological context is critical for understanding the causes and consequences of innovation. By including two species, we demonstrate that cooperation and competition across several biological scales shapes the origin and persistence of multicellularity.},
}
RevDate: 2023-09-18
Programmed Cell Death in Unicellular Versus Multicellular Organisms.
Annual review of genetics [Epub ahead of print].
Programmed cell death (self-induced) is intrinsic to all cellular life forms, including unicellular organisms. However, cell death research has focused on animal models to understand cancer, degenerative disorders, and developmental processes. Recently delineated suicidal death mechanisms in bacteria and fungi have revealed ancient origins of animal cell death that are intertwined with immune mechanisms, allaying earlier doubts that self-inflicted cell death pathways exist in microorganisms. Approximately 20 mammalian death pathways have been partially characterized over the last 35 years. By contrast, more than 100 death mechanisms have been identified in bacteria and a few fungi in recent years. However, cell death is nearly unstudied in most human pathogenic microbes that cause major public health burdens. Here, we consider how the current understanding of programmed cell death arose through animal studies and how recently uncovered microbial cell death mechanisms in fungi and bacteria resemble and differ from mechanisms of mammalian cell death. Expected final online publication date for the Annual Review of Genetics, Volume 57 is November 2023. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
Additional Links: PMID-37722687
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@article {pmid37722687,
year = {2023},
author = {Kulkarni, M and Hardwick, JM},
title = {Programmed Cell Death in Unicellular Versus Multicellular Organisms.},
journal = {Annual review of genetics},
volume = {},
number = {},
pages = {},
doi = {10.1146/annurev-genet-033123-095833},
pmid = {37722687},
issn = {1545-2948},
abstract = {Programmed cell death (self-induced) is intrinsic to all cellular life forms, including unicellular organisms. However, cell death research has focused on animal models to understand cancer, degenerative disorders, and developmental processes. Recently delineated suicidal death mechanisms in bacteria and fungi have revealed ancient origins of animal cell death that are intertwined with immune mechanisms, allaying earlier doubts that self-inflicted cell death pathways exist in microorganisms. Approximately 20 mammalian death pathways have been partially characterized over the last 35 years. By contrast, more than 100 death mechanisms have been identified in bacteria and a few fungi in recent years. However, cell death is nearly unstudied in most human pathogenic microbes that cause major public health burdens. Here, we consider how the current understanding of programmed cell death arose through animal studies and how recently uncovered microbial cell death mechanisms in fungi and bacteria resemble and differ from mechanisms of mammalian cell death. Expected final online publication date for the Annual Review of Genetics, Volume 57 is November 2023. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.},
}
RevDate: 2023-09-12
Evolution: The ancient history of cilia assembly regulation.
Current biology : CB, 33(17):R898-R900.
A new study identifies a conserved regulatory mechanism for cilia assembly in the closest unicellular relatives of animals, suggesting that this mechanism was already present in a common unicellular ancestor and was repurposed during the transition to multicellularity.
Additional Links: PMID-37699344
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@article {pmid37699344,
year = {2023},
author = {Azimzadeh, J and Durand, B},
title = {Evolution: The ancient history of cilia assembly regulation.},
journal = {Current biology : CB},
volume = {33},
number = {17},
pages = {R898-R900},
doi = {10.1016/j.cub.2023.07.053},
pmid = {37699344},
issn = {1879-0445},
abstract = {A new study identifies a conserved regulatory mechanism for cilia assembly in the closest unicellular relatives of animals, suggesting that this mechanism was already present in a common unicellular ancestor and was repurposed during the transition to multicellularity.},
}
RevDate: 2023-09-07
Integrins and their potential roles in mammalian pregnancy.
Journal of animal science and biotechnology, 14(1):115.
Integrins are a highly complex family of receptors that, when expressed on the surface of cells, can mediate reciprocal cell-to-cell and cell-to-extracellular matrix (ECM) interactions leading to assembly of integrin adhesion complexes (IACs) that initiate many signaling functions both at the membrane and deeper within the cytoplasm to coordinate processes including cell adhesion, migration, proliferation, survival, differentiation, and metabolism. All metazoan organisms possess integrins, and it is generally agreed that integrins were associated with the evolution of multicellularity, being essential for the association of cells with their neighbors and surroundings, during embryonic development and many aspects of cellular and molecular biology. Integrins have important roles in many aspects of embryonic development, normal physiology, and disease processes with a multitude of functions discovered and elucidated for integrins that directly influence many areas of biology and medicine, including mammalian pregnancy, in particular implantation of the blastocyst to the uterine wall, subsequent placentation and conceptus (embryo/fetus and associated placental membranes) development. This review provides a succinct overview of integrin structure, ligand binding, and signaling followed with a concise overview of embryonic development, implantation, and early placentation in pigs, sheep, humans, and mice as an example for rodents. A brief timeline of the initial localization of integrin subunits to the uterine luminal epithelium (LE) and conceptus trophoblast is then presented, followed by sequential summaries of integrin expression and function during gestation in pigs, sheep, humans, and rodents. As appropriate for this journal, summaries of integrin expression and function during gestation in pigs and sheep are in depth, whereas summaries for humans and rodents are brief. Because similar models to those illustrated in Fig. 1, 2, 3, 4, 5 and 6 are present throughout the scientific literature, the illustrations in this manuscript are drafted as Viking imagery for entertainment purposes.
Additional Links: PMID-37679778
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@article {pmid37679778,
year = {2023},
author = {Johnson, GA and Burghardt, RC and Bazer, FW and Seo, H and Cain, JW},
title = {Integrins and their potential roles in mammalian pregnancy.},
journal = {Journal of animal science and biotechnology},
volume = {14},
number = {1},
pages = {115},
pmid = {37679778},
issn = {1674-9782},
support = {98-35203-6337//National Institute of Food and Agriculture/ ; 2006-35203-17199//National Institute of Food and Agriculture/ ; 2012-67011-19892//National Institute of Food and Agriculture/ ; 2016-67015-24955//National Institute of Food and Agriculture/ ; 1-F32-HDO 8501 O1A1//Eunice Kennedy Shriver National Institute of Child Health and Human Development/ ; 1R21HD071468-01//Eunice Kennedy Shriver National Institute of Child Health and Human Development/ ; },
abstract = {Integrins are a highly complex family of receptors that, when expressed on the surface of cells, can mediate reciprocal cell-to-cell and cell-to-extracellular matrix (ECM) interactions leading to assembly of integrin adhesion complexes (IACs) that initiate many signaling functions both at the membrane and deeper within the cytoplasm to coordinate processes including cell adhesion, migration, proliferation, survival, differentiation, and metabolism. All metazoan organisms possess integrins, and it is generally agreed that integrins were associated with the evolution of multicellularity, being essential for the association of cells with their neighbors and surroundings, during embryonic development and many aspects of cellular and molecular biology. Integrins have important roles in many aspects of embryonic development, normal physiology, and disease processes with a multitude of functions discovered and elucidated for integrins that directly influence many areas of biology and medicine, including mammalian pregnancy, in particular implantation of the blastocyst to the uterine wall, subsequent placentation and conceptus (embryo/fetus and associated placental membranes) development. This review provides a succinct overview of integrin structure, ligand binding, and signaling followed with a concise overview of embryonic development, implantation, and early placentation in pigs, sheep, humans, and mice as an example for rodents. A brief timeline of the initial localization of integrin subunits to the uterine luminal epithelium (LE) and conceptus trophoblast is then presented, followed by sequential summaries of integrin expression and function during gestation in pigs, sheep, humans, and rodents. As appropriate for this journal, summaries of integrin expression and function during gestation in pigs and sheep are in depth, whereas summaries for humans and rodents are brief. Because similar models to those illustrated in Fig. 1, 2, 3, 4, 5 and 6 are present throughout the scientific literature, the illustrations in this manuscript are drafted as Viking imagery for entertainment purposes.},
}
RevDate: 2023-09-07
Why is chronic kidney disease progressive? Evolutionary adaptations and maladaptations.
American journal of physiology. Renal physiology [Epub ahead of print].
Despite significant advances in renal physiology, the global prevalence of chronic kidney disease (CKD) continues to increase. The emergence of multicellular organisms gave rise to increasing complexity of life resulting in tradeoffs reflecting ancestral adaptations to changing environments. Three evolutionary traits shape CKD over the lifespan: 1) variation in nephron number at birth, 2) progressive nephron loss with aging, and 3) adaptive kidney growth in response to decreased nephron number. Although providing plasticity in adaptation to changing environments, the cell cycle must function within constraints dictated by available energy. Prioritized allocation of energy available through the placenta can restrict fetal nephrogenesis, a risk factor for CKD. Moreover, nephron loss with aging is a consequence of cell senescence, a pathway accelerated by adaptive nephron hypertrophy that maintains metabolic homeostasis at the expense of increased vulnerability to stressors. Driven by reproductive fitness, natural selection operates in early life, but diminishes thereafter, leading to an exponential increase in CKD with aging, a product of antagonistic pleiotropy. A deeper understanding of the evolutionary constraints on the cell cycle may lead to manipulation of the balance between progenitor cell renewal and differentiation, regulation of cell senescence, and modulation of the balance between cell proliferation and hypertrophy. Application of an evolutionary perspective may enhance understanding of adaptation and maladaptation by nephrons in the progression of CKD, leading to new therapeutic advances.
Additional Links: PMID-37675460
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@article {pmid37675460,
year = {2023},
author = {Chevalier, RL},
title = {Why is chronic kidney disease progressive? Evolutionary adaptations and maladaptations.},
journal = {American journal of physiology. Renal physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajprenal.00134.2023},
pmid = {37675460},
issn = {1522-1466},
abstract = {Despite significant advances in renal physiology, the global prevalence of chronic kidney disease (CKD) continues to increase. The emergence of multicellular organisms gave rise to increasing complexity of life resulting in tradeoffs reflecting ancestral adaptations to changing environments. Three evolutionary traits shape CKD over the lifespan: 1) variation in nephron number at birth, 2) progressive nephron loss with aging, and 3) adaptive kidney growth in response to decreased nephron number. Although providing plasticity in adaptation to changing environments, the cell cycle must function within constraints dictated by available energy. Prioritized allocation of energy available through the placenta can restrict fetal nephrogenesis, a risk factor for CKD. Moreover, nephron loss with aging is a consequence of cell senescence, a pathway accelerated by adaptive nephron hypertrophy that maintains metabolic homeostasis at the expense of increased vulnerability to stressors. Driven by reproductive fitness, natural selection operates in early life, but diminishes thereafter, leading to an exponential increase in CKD with aging, a product of antagonistic pleiotropy. A deeper understanding of the evolutionary constraints on the cell cycle may lead to manipulation of the balance between progenitor cell renewal and differentiation, regulation of cell senescence, and modulation of the balance between cell proliferation and hypertrophy. Application of an evolutionary perspective may enhance understanding of adaptation and maladaptation by nephrons in the progression of CKD, leading to new therapeutic advances.},
}
RevDate: 2023-09-05
Targeted Hypermutation as a Survival Strategy: A Theoretical Approach.
Acta biotheoretica, 71(4):20.
Targeted hypermutation has proven to be a useful survival strategy for bacteria under severe stress and is also used by multicellular organisms in specific instances such as the mammalian immune system. This might appear surprising, given the generally observed deleterious effects of poor replication fidelity/high mutation rate. A previous theoretical model designed to explore the role of replication fidelity in the origin of life was applied to a simulated hypermutation scenario. The results confirmed that the same model is useful for analyzing hypermutation and can predict the effects of the same parameters (survival probability, replication fidelity, mutation effect, and others) on the survival of cellular populations undergoing hypermutation as a result of severe stress.
Additional Links: PMID-37668864
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@article {pmid37668864,
year = {2023},
author = {Garte, S},
title = {Targeted Hypermutation as a Survival Strategy: A Theoretical Approach.},
journal = {Acta biotheoretica},
volume = {71},
number = {4},
pages = {20},
pmid = {37668864},
issn = {1572-8358},
abstract = {Targeted hypermutation has proven to be a useful survival strategy for bacteria under severe stress and is also used by multicellular organisms in specific instances such as the mammalian immune system. This might appear surprising, given the generally observed deleterious effects of poor replication fidelity/high mutation rate. A previous theoretical model designed to explore the role of replication fidelity in the origin of life was applied to a simulated hypermutation scenario. The results confirmed that the same model is useful for analyzing hypermutation and can predict the effects of the same parameters (survival probability, replication fidelity, mutation effect, and others) on the survival of cellular populations undergoing hypermutation as a result of severe stress.},
}
RevDate: 2023-09-04
Evolution of phenotypic disparity in the plant kingdom.
Nature plants [Epub ahead of print].
The plant kingdom exhibits diverse bodyplans, from single-celled algae to complex multicellular land plants, but it is unclear how this phenotypic disparity was achieved. Here we show that the living divisions comprise discrete clusters within morphospace, separated largely by reproductive innovations, the extinction of evolutionary intermediates and lineage-specific evolution. Phenotypic complexity correlates not with disparity but with ploidy history, reflecting the role of genome duplication in plant macroevolution. Overall, the plant kingdom exhibits a pattern of episodically increasing disparity throughout its evolutionary history that mirrors the evolutionary floras and reflects ecological expansion facilitated by reproductive innovations. This pattern also parallels that seen in the animal and fungal kingdoms, suggesting a general pattern for the evolution of multicellular bodyplans.
Additional Links: PMID-37666963
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@article {pmid37666963,
year = {2023},
author = {Clark, JW and Hetherington, AJ and Morris, JL and Pressel, S and Duckett, JG and Puttick, MN and Schneider, H and Kenrick, P and Wellman, CH and Donoghue, PCJ},
title = {Evolution of phenotypic disparity in the plant kingdom.},
journal = {Nature plants},
volume = {},
number = {},
pages = {},
pmid = {37666963},
issn = {2055-0278},
support = {NE/N002067/1//RCUK | Natural Environment Research Council (NERC)/ ; NE/P013678/1//RCUK | Natural Environment Research Council (NERC)/ ; NE/N002067/1//RCUK | Natural Environment Research Council (NERC)/ ; NE/N002067/1//RCUK | Natural Environment Research Council (NERC)/ ; NE/N002067/1//RCUK | Natural Environment Research Council (NERC)/ ; NE/N002067/1//RCUK | Natural Environment Research Council (NERC)/ ; NE/N002067/1//RCUK | Natural Environment Research Council (NERC)/ ; NE/N002067/1//RCUK | Natural Environment Research Council (NERC)/ ; NE/N002067/1//RCUK | Natural Environment Research Council (NERC)/ ; BB/N000919/1//RCUK | Biotechnology and Biological Sciences Research Council (BBSRC)/ ; BB/T012773/1//RCUK | Biotechnology and Biological Sciences Research Council (BBSRC)/ ; RF-2022-167//Leverhulme Trust/ ; RPG-2019-004//Leverhulme Trust/ ; JTF 62574//John Templeton Foundation (JTF)/ ; },
abstract = {The plant kingdom exhibits diverse bodyplans, from single-celled algae to complex multicellular land plants, but it is unclear how this phenotypic disparity was achieved. Here we show that the living divisions comprise discrete clusters within morphospace, separated largely by reproductive innovations, the extinction of evolutionary intermediates and lineage-specific evolution. Phenotypic complexity correlates not with disparity but with ploidy history, reflecting the role of genome duplication in plant macroevolution. Overall, the plant kingdom exhibits a pattern of episodically increasing disparity throughout its evolutionary history that mirrors the evolutionary floras and reflects ecological expansion facilitated by reproductive innovations. This pattern also parallels that seen in the animal and fungal kingdoms, suggesting a general pattern for the evolution of multicellular bodyplans.},
}
RevDate: 2023-09-04
Editorial: Unicellular organisms as an evolutionary snapshot toward multicellularity.
Frontiers in cell and developmental biology, 11:1254636.
Additional Links: PMID-37664459
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@article {pmid37664459,
year = {2023},
author = {Marotta, P and Ruggiero, A and Bilcke, G},
title = {Editorial: Unicellular organisms as an evolutionary snapshot toward multicellularity.},
journal = {Frontiers in cell and developmental biology},
volume = {11},
number = {},
pages = {1254636},
pmid = {37664459},
issn = {2296-634X},
}
RevDate: 2023-09-04
Maintaining, masking, and mimicking selection: the interplay of cell-intrinsic and cell-extrinsic effects upon eco-evolutionary dynamics.
bioRxiv : the preprint server for biology pii:2023.03.15.532871.
Evolution is a stochastic yet inevitable process that lies at the heart of biology yet in the multi-cellular environments within patients, ecological complexities arise via heterogeneity and microenvironments. The interplay of ecology and mutation is thus fundamental to predicting the evolution of complex diseases and engineering optimal treatment solutions. As experimental evidence of ecological interactions between disease agents continues to grow, so does the need for evolutionary theory and modeling that incorporates these interaction effects. Inspired by experimental cell biology, we transform the variables in the interaction payoff matrix to encode cell-cell interactions in our mathematical approach as growth-rate modifying, frequency-dependent interactions. In this way, we can show the extent to which the presence of these cell-extrinsic ecological interactions can modify the evolutionary trajectories that would be predicted from cell-intrinsic properties alone. To do this we form a Fokker-Planck equation for a genetic population undergoing diffusion, drift, and interactions and generate a novel, analytic solution for the stationary distribution. We use this solution to determine when these interactions can modify evolution in such ways as to maintain, mask, or mimic mono-culture fitness differences. This work has implications for the interpretation and understanding of experimental and patient evolution and is a result that may help to explain the abundance of apparently neutral evolution in cancer systems and heterogeneous populations in general. In addition, the derivation of an analytical result for stochastic, ecologically dependent evolution paves the way for treatment approaches requiring knowledge of a stationary solution for the development of control protocols.
Additional Links: PMID-36993598
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@article {pmid36993598,
year = {2023},
author = {Barker-Clarke, RJ and Gray, JM and Tadele, DS and Hinczewski, M and Scott, JG},
title = {Maintaining, masking, and mimicking selection: the interplay of cell-intrinsic and cell-extrinsic effects upon eco-evolutionary dynamics.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2023.03.15.532871},
pmid = {36993598},
support = {R37 CA244613/CA/NCI NIH HHS/United States ; },
abstract = {Evolution is a stochastic yet inevitable process that lies at the heart of biology yet in the multi-cellular environments within patients, ecological complexities arise via heterogeneity and microenvironments. The interplay of ecology and mutation is thus fundamental to predicting the evolution of complex diseases and engineering optimal treatment solutions. As experimental evidence of ecological interactions between disease agents continues to grow, so does the need for evolutionary theory and modeling that incorporates these interaction effects. Inspired by experimental cell biology, we transform the variables in the interaction payoff matrix to encode cell-cell interactions in our mathematical approach as growth-rate modifying, frequency-dependent interactions. In this way, we can show the extent to which the presence of these cell-extrinsic ecological interactions can modify the evolutionary trajectories that would be predicted from cell-intrinsic properties alone. To do this we form a Fokker-Planck equation for a genetic population undergoing diffusion, drift, and interactions and generate a novel, analytic solution for the stationary distribution. We use this solution to determine when these interactions can modify evolution in such ways as to maintain, mask, or mimic mono-culture fitness differences. This work has implications for the interpretation and understanding of experimental and patient evolution and is a result that may help to explain the abundance of apparently neutral evolution in cancer systems and heterogeneous populations in general. In addition, the derivation of an analytical result for stochastic, ecologically dependent evolution paves the way for treatment approaches requiring knowledge of a stationary solution for the development of control protocols.},
}
RevDate: 2023-08-31
Red macroalgae in the genomic era.
The New phytologist [Epub ahead of print].
Rhodophyta (or red algae) are a diverse and species-rich group that forms one of three major lineages in the Archaeplastida, a eukaryotic supergroup whose plastids arose from a single primary endosymbiosis. Red algae are united by several features, such as relatively small intron-poor genomes and a lack of cytoskeletal structures associated with motility like flagella and centrioles, as well as a highly efficient photosynthetic capacity. Multicellular red algae (or macroalgae) are one of the earliest diverging eukaryotic lineages to have evolved complex multicellularity, yet despite their ecological, evolutionary, and commercial importance, they have remained a largely understudied group of organisms. Considering the increasing availability of red algal genome sequences, we present a broad overview of fundamental aspects of red macroalgal biology and posit on how this is expected to accelerate research in many domains of red algal biology in the coming years.
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@article {pmid37649301,
year = {2023},
author = {Borg, M and Krueger-Hadfield, SA and Destombe, C and Collén, J and Lipinska, A and Coelho, SM},
title = {Red macroalgae in the genomic era.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.19211},
pmid = {37649301},
issn = {1469-8137},
support = {//Bettencourt Schuller Foundation/ ; //Gordon and Betty Moore Foundation/ ; 864038//H2020 European Research Council/ ; DEB-2141971//National Science Foundation/ ; //Max Planck Society/ ; },
abstract = {Rhodophyta (or red algae) are a diverse and species-rich group that forms one of three major lineages in the Archaeplastida, a eukaryotic supergroup whose plastids arose from a single primary endosymbiosis. Red algae are united by several features, such as relatively small intron-poor genomes and a lack of cytoskeletal structures associated with motility like flagella and centrioles, as well as a highly efficient photosynthetic capacity. Multicellular red algae (or macroalgae) are one of the earliest diverging eukaryotic lineages to have evolved complex multicellularity, yet despite their ecological, evolutionary, and commercial importance, they have remained a largely understudied group of organisms. Considering the increasing availability of red algal genome sequences, we present a broad overview of fundamental aspects of red macroalgal biology and posit on how this is expected to accelerate research in many domains of red algal biology in the coming years.},
}
RevDate: 2023-08-30
Phylogeny-wide analysis of G-protein coupled receptors in social amoebas and implications for the evolution of multicellularity.
Open research Europe, 2:134.
G-protein coupled receptors (GPCRs) are seven-transmembrane proteins and constitute the largest group of receptors within eukaryotes. The presence of a large set of GPCRs in the unicellular Amoebozoa was surprising and is indicative of the largely undiscovered environmental sensing capabilities in this group. Evolutionary transitions from unicellular to multicellular lifestyles, like we see in social amoebas, have occurred several times independently in the Amoebozoa, and GPCRs may have been co-opted for new functions in cell-cell communication. Methods We have analysed a set of GPCRs from fully sequenced Amoebozoan genomes by Bayesian inference, compared their phylogenetic distribution and domain composition, and analysed their temporal and spatial expression patterns in five species of dictyostelids. Results We found evidence that most GPCRs are conserved deeply in the Amoebozoa and are probably performing roles in general cell functions and complex environmental sensing. All families of GPCRs (apart from the family 4 fungal pheromone receptors) are present in dictyostelids with family 5 being the largest and family 2 the one with the fewest members. For the first time, we identify the presence of family 1 rhodopsin-like GPCRs in dictyostelids. Some GPCRs have been amplified in the dictyostelids and in specific lineages thereof and through changes in expression patterns may have been repurposed for signalling in multicellular development. Discussion Our phylogenetic analysis suggests that GPCR families 1, 2 and 6 already diverged early in the Amoebozoa, whereas families 3 and 5 expanded later within the dictyostelids. The family 6 cAMP receptors that have experimentally supported roles in multicellular development in dictyostelids (carA-carD; tasA/B) originated at the root of all dictyostelids and only have weakly associated homologs in Physarum polycephalum. Our analysis identified candidate GPCRs which have evolved in the dictyostelids and could have been co-opted for multicellular development.
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@article {pmid37645274,
year = {2022},
author = {Hall, G and Kelly, S and Schaap, P and Schilde, C},
title = {Phylogeny-wide analysis of G-protein coupled receptors in social amoebas and implications for the evolution of multicellularity.},
journal = {Open research Europe},
volume = {2},
number = {},
pages = {134},
pmid = {37645274},
issn = {2732-5121},
abstract = {G-protein coupled receptors (GPCRs) are seven-transmembrane proteins and constitute the largest group of receptors within eukaryotes. The presence of a large set of GPCRs in the unicellular Amoebozoa was surprising and is indicative of the largely undiscovered environmental sensing capabilities in this group. Evolutionary transitions from unicellular to multicellular lifestyles, like we see in social amoebas, have occurred several times independently in the Amoebozoa, and GPCRs may have been co-opted for new functions in cell-cell communication. Methods We have analysed a set of GPCRs from fully sequenced Amoebozoan genomes by Bayesian inference, compared their phylogenetic distribution and domain composition, and analysed their temporal and spatial expression patterns in five species of dictyostelids. Results We found evidence that most GPCRs are conserved deeply in the Amoebozoa and are probably performing roles in general cell functions and complex environmental sensing. All families of GPCRs (apart from the family 4 fungal pheromone receptors) are present in dictyostelids with family 5 being the largest and family 2 the one with the fewest members. For the first time, we identify the presence of family 1 rhodopsin-like GPCRs in dictyostelids. Some GPCRs have been amplified in the dictyostelids and in specific lineages thereof and through changes in expression patterns may have been repurposed for signalling in multicellular development. Discussion Our phylogenetic analysis suggests that GPCR families 1, 2 and 6 already diverged early in the Amoebozoa, whereas families 3 and 5 expanded later within the dictyostelids. The family 6 cAMP receptors that have experimentally supported roles in multicellular development in dictyostelids (carA-carD; tasA/B) originated at the root of all dictyostelids and only have weakly associated homologs in Physarum polycephalum. Our analysis identified candidate GPCRs which have evolved in the dictyostelids and could have been co-opted for multicellular development.},
}
RevDate: 2023-08-26
Spontaneous Emergence of Multicellular Heritability.
Genes, 14(8): pii:genes14081635.
The major transitions in evolution include events and processes that result in the emergence of new levels of biological individuality. For collectives to undergo Darwinian evolution, their traits must be heritable, but the emergence of higher-level heritability is poorly understood and has long been considered a stumbling block for nascent evolutionary transitions. Using analytical models, synthetic biology, and biologically-informed simulations, we explored the emergence of trait heritability during the evolution of multicellularity. Prior work on the evolution of multicellularity has asserted that substantial collective-level trait heritability either emerges only late in the transition or requires some evolutionary change subsequent to the formation of clonal multicellular groups. In a prior analytical model, we showed that collective-level heritability not only exists but is usually more heritable than the underlying cell-level trait upon which it is based, as soon as multicellular groups form. Here, we show that key assumptions and predictions of that model are borne out in a real engineered biological system, with important implications for the emergence of collective-level heritability.
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@article {pmid37628687,
year = {2023},
author = {Zamani-Dahaj, SA and Burnetti, A and Day, TC and Yunker, PJ and Ratcliff, WC and Herron, MD},
title = {Spontaneous Emergence of Multicellular Heritability.},
journal = {Genes},
volume = {14},
number = {8},
pages = {},
doi = {10.3390/genes14081635},
pmid = {37628687},
issn = {2073-4425},
support = {GM138030/GM/NIGMS NIH HHS/United States ; NNA17BB05A/NASA/NASA/United States ; },
abstract = {The major transitions in evolution include events and processes that result in the emergence of new levels of biological individuality. For collectives to undergo Darwinian evolution, their traits must be heritable, but the emergence of higher-level heritability is poorly understood and has long been considered a stumbling block for nascent evolutionary transitions. Using analytical models, synthetic biology, and biologically-informed simulations, we explored the emergence of trait heritability during the evolution of multicellularity. Prior work on the evolution of multicellularity has asserted that substantial collective-level trait heritability either emerges only late in the transition or requires some evolutionary change subsequent to the formation of clonal multicellular groups. In a prior analytical model, we showed that collective-level heritability not only exists but is usually more heritable than the underlying cell-level trait upon which it is based, as soon as multicellular groups form. Here, we show that key assumptions and predictions of that model are borne out in a real engineered biological system, with important implications for the emergence of collective-level heritability.},
}
RevDate: 2023-08-24
Phenotype Design Space Provides a Mechanistic Framework Relating Molecular Parameters to Phenotype Diversity Available for Selection.
Journal of molecular evolution [Epub ahead of print].
Two long-standing challenges in theoretical population genetics and evolution are predicting the distribution of phenotype diversity generated by mutation and available for selection, and determining the interaction of mutation, selection and drift to characterize evolutionary equilibria and dynamics. More fundamental for enabling such predictions is the current inability to causally link genotype to phenotype. There are three major mechanistic mappings required for such a linking - genetic sequence to kinetic parameters of the molecular processes, kinetic parameters to biochemical system phenotypes, and biochemical phenotypes to organismal phenotypes. This article introduces a theoretical framework, the Phenotype Design Space (PDS) framework, for addressing these challenges by focusing on the mapping of kinetic parameters to biochemical system phenotypes. It provides a quantitative theory whose key features include (1) a mathematically rigorous definition of phenotype based on biochemical kinetics, (2) enumeration of the full phenotypic repertoire, and (3) functional characterization of each phenotype independent of its context-dependent selection or fitness contributions. This framework is built on Design Space methods that relate system phenotypes to genetically determined parameters and environmentally determined variables. It also has the potential to automate prediction of phenotype-specific mutation rate constants and equilibrium distributions of phenotype diversity in microbial populations undergoing steady-state exponential growth, which provides an ideal reference to which more realistic cases can be compared. Although the framework is quite general and flexible, the details will undoubtedly differ for different functions, organisms and contexts. Here a hypothetical case study involving a small molecular system, a primordial circadian clock, is used to introduce this framework and to illustrate its use in a particular case. The framework is built on fundamental biochemical kinetics. Thus, the foundation is based on linear algebra and reasonable physical assumptions, which provide numerous opportunities for experimental testing and further elaboration to deal with complex multicellular organisms that are currently beyond its scope. The discussion provides a comparison of results from the PDS framework with those from other approaches in theoretical population genetics.
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@article {pmid37620617,
year = {2023},
author = {Savageau, MA},
title = {Phenotype Design Space Provides a Mechanistic Framework Relating Molecular Parameters to Phenotype Diversity Available for Selection.},
journal = {Journal of molecular evolution},
volume = {},
number = {},
pages = {},
pmid = {37620617},
issn = {1432-1432},
support = {MCB 1716833//National Science Foundation/ ; },
abstract = {Two long-standing challenges in theoretical population genetics and evolution are predicting the distribution of phenotype diversity generated by mutation and available for selection, and determining the interaction of mutation, selection and drift to characterize evolutionary equilibria and dynamics. More fundamental for enabling such predictions is the current inability to causally link genotype to phenotype. There are three major mechanistic mappings required for such a linking - genetic sequence to kinetic parameters of the molecular processes, kinetic parameters to biochemical system phenotypes, and biochemical phenotypes to organismal phenotypes. This article introduces a theoretical framework, the Phenotype Design Space (PDS) framework, for addressing these challenges by focusing on the mapping of kinetic parameters to biochemical system phenotypes. It provides a quantitative theory whose key features include (1) a mathematically rigorous definition of phenotype based on biochemical kinetics, (2) enumeration of the full phenotypic repertoire, and (3) functional characterization of each phenotype independent of its context-dependent selection or fitness contributions. This framework is built on Design Space methods that relate system phenotypes to genetically determined parameters and environmentally determined variables. It also has the potential to automate prediction of phenotype-specific mutation rate constants and equilibrium distributions of phenotype diversity in microbial populations undergoing steady-state exponential growth, which provides an ideal reference to which more realistic cases can be compared. Although the framework is quite general and flexible, the details will undoubtedly differ for different functions, organisms and contexts. Here a hypothetical case study involving a small molecular system, a primordial circadian clock, is used to introduce this framework and to illustrate its use in a particular case. The framework is built on fundamental biochemical kinetics. Thus, the foundation is based on linear algebra and reasonable physical assumptions, which provide numerous opportunities for experimental testing and further elaboration to deal with complex multicellular organisms that are currently beyond its scope. The discussion provides a comparison of results from the PDS framework with those from other approaches in theoretical population genetics.},
}
RevDate: 2023-08-24
Genome analysis of Tepidibacter sp. SWIR-1, an anaerobic endospore-forming bacterium isolated from a deep-sea hydrothermal vent.
Marine genomics, 71:101049.
Tepidibacter sp. SWIR-1, a putative new species isolated from deep-sea hydrothermal vent field on the Southwest Indian Ridge (SWIR), is an anaerobic, mesophilic and endospore-forming bacterium belonging to the family Peptostreptococcaceae. In this study, we present the complete genome sequence of strain SWIR-1, consists of a single circular chromosome comprising 4,122,966 nucleotides with 29.25% G + C content and a circular plasmid comprising 38,843 nucleotides with 29.46% G + C content. In total, 3861 protein coding genes, 104 tRNA genes and 46 rRNA genes were obtained. SWIR-1 genome contains numerous genes related to sporulation and germination. Compared with the other three Tepidibacter species, SWIR-1 contained more spore germination receptor proteins. In addition, SWIR-1 contained more genes involved in chemotaxis and two-component systems than other Tepidibacter species. These results indicated that SWIR-1 has developed versatile adaptability to the Southwest Indian Ridge hydrothermal vent environment. The genome of strain SWIR-1 will be helpful for further understanding adaptive strategies used by bacteria dwelling in the deep-sea hydrothermal vent environments of different oceans.
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@article {pmid37620056,
year = {2023},
author = {Li, XG and Dai, J and Zhang, WJ and Jiang, AJ and Li, DH and Wu, LF},
title = {Genome analysis of Tepidibacter sp. SWIR-1, an anaerobic endospore-forming bacterium isolated from a deep-sea hydrothermal vent.},
journal = {Marine genomics},
volume = {71},
number = {},
pages = {101049},
doi = {10.1016/j.margen.2023.101049},
pmid = {37620056},
issn = {1876-7478},
abstract = {Tepidibacter sp. SWIR-1, a putative new species isolated from deep-sea hydrothermal vent field on the Southwest Indian Ridge (SWIR), is an anaerobic, mesophilic and endospore-forming bacterium belonging to the family Peptostreptococcaceae. In this study, we present the complete genome sequence of strain SWIR-1, consists of a single circular chromosome comprising 4,122,966 nucleotides with 29.25% G + C content and a circular plasmid comprising 38,843 nucleotides with 29.46% G + C content. In total, 3861 protein coding genes, 104 tRNA genes and 46 rRNA genes were obtained. SWIR-1 genome contains numerous genes related to sporulation and germination. Compared with the other three Tepidibacter species, SWIR-1 contained more spore germination receptor proteins. In addition, SWIR-1 contained more genes involved in chemotaxis and two-component systems than other Tepidibacter species. These results indicated that SWIR-1 has developed versatile adaptability to the Southwest Indian Ridge hydrothermal vent environment. The genome of strain SWIR-1 will be helpful for further understanding adaptive strategies used by bacteria dwelling in the deep-sea hydrothermal vent environments of different oceans.},
}
RevDate: 2023-08-23
Post-insemination sexual selection in males indirectly masculinizes the female transcriptome.
bioRxiv : the preprint server for biology pii:2023.08.09.552689.
UNLABELLED: Sex-specific regulation of gene expression is the most plausible way for generating sexually differentiated phenotypes from an essentially shared genome. However, since genetic material is shared, sex-specific selection in one sex can have an indirect response in the other sex. From a gene expression perspective, this tethered response can move one sex away from their wildtype expression state and impact potentially many gene regulatory networks. Here, using experimental evolution in the model nematode Caenorhabditis elegans , we explore the coupling of direct sexual selection on males with the transcriptomic response in females over microevolutionary timescales to uncover the extent to which post-insemination reproductive traits share a genetic basis between the sexes. We find that differential gene expression is driven by female ancestral or evolved generation alone and that male generation has no impact on changes in gene expression. Almost all differentially expressed genes were downregulated in evolved females. Moreover, 80% of these gene were located on the X chromosome and have wildtype female-biased expression profiles. Changes in gene expression profiles were likely driven through trans -acting pathways that are shared between the sexes. We found no evidence that the core dosage compensation machinery was impacted by experimental evolution. Together these data suggest masculinization of the female transcriptome driven by direct selection on male sperm competitive ability. Our results indicate that on short evolutionary timescales sexual selection can generate sexual conflict in expression space.
LAY SUMMARY: Sexual selection drives the evolution of some of the most dramatic phenotypic differences between the sexes. Such sexual dimorphism is so common across multicellular organisms that we often overlook how remarkable it is for shared genetic material to create numerous and complex sex differences. At an evolutionary level, sexual dimorphism furthers the opportunity for sex-specific selection to optimize the fitness of a given sex. As a consequence, sex-specific selection, such as sexual selection, can have an indirect evolutionary response in the other sex due to genetic associations created by the sexes sharing the same genome. This correlated evolutionary response can create sexual conflict by shifting a sex away from their fitness optimum. At the functional level, sexual dimorphism is generated is through sex-specific regulation of gene expression. Bridging the evolutionary response to sexual selection with the evolution of sex-specific gene regulation during post-mating interactions has proved challenging. We previously used experimental evolution to increase male fertility by directly selecting for increased sperm competitive ability. In this study, we examined the effect of this direct selection on males on gene expression patterns in females. Differential gene expression was determined by whether a female was ancestral or evolved generation, indicating that gene expression changes were an evolved response due to indirect selection on females. Significantly differentially expressed genes were downregulated in evolved females. These genes tended to be female-biased in wildtype individuals and located on the X chromosome. The downregulation of X-linked genes suggests expression levels in females equal to or lower than that in males. Together these results indicate a less female-like transcriptome after experimental evolution. This supports a sexual conflict scenario by which direct sexual selection on males indirectly masculinizes the female transcriptome over short evolutionary timescales.
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@article {pmid37609247,
year = {2023},
author = {Kasimatis, KR and Willis, JH and Phillips, PC},
title = {Post-insemination sexual selection in males indirectly masculinizes the female transcriptome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2023.08.09.552689},
pmid = {37609247},
abstract = {UNLABELLED: Sex-specific regulation of gene expression is the most plausible way for generating sexually differentiated phenotypes from an essentially shared genome. However, since genetic material is shared, sex-specific selection in one sex can have an indirect response in the other sex. From a gene expression perspective, this tethered response can move one sex away from their wildtype expression state and impact potentially many gene regulatory networks. Here, using experimental evolution in the model nematode Caenorhabditis elegans , we explore the coupling of direct sexual selection on males with the transcriptomic response in females over microevolutionary timescales to uncover the extent to which post-insemination reproductive traits share a genetic basis between the sexes. We find that differential gene expression is driven by female ancestral or evolved generation alone and that male generation has no impact on changes in gene expression. Almost all differentially expressed genes were downregulated in evolved females. Moreover, 80% of these gene were located on the X chromosome and have wildtype female-biased expression profiles. Changes in gene expression profiles were likely driven through trans -acting pathways that are shared between the sexes. We found no evidence that the core dosage compensation machinery was impacted by experimental evolution. Together these data suggest masculinization of the female transcriptome driven by direct selection on male sperm competitive ability. Our results indicate that on short evolutionary timescales sexual selection can generate sexual conflict in expression space.
LAY SUMMARY: Sexual selection drives the evolution of some of the most dramatic phenotypic differences between the sexes. Such sexual dimorphism is so common across multicellular organisms that we often overlook how remarkable it is for shared genetic material to create numerous and complex sex differences. At an evolutionary level, sexual dimorphism furthers the opportunity for sex-specific selection to optimize the fitness of a given sex. As a consequence, sex-specific selection, such as sexual selection, can have an indirect evolutionary response in the other sex due to genetic associations created by the sexes sharing the same genome. This correlated evolutionary response can create sexual conflict by shifting a sex away from their fitness optimum. At the functional level, sexual dimorphism is generated is through sex-specific regulation of gene expression. Bridging the evolutionary response to sexual selection with the evolution of sex-specific gene regulation during post-mating interactions has proved challenging. We previously used experimental evolution to increase male fertility by directly selecting for increased sperm competitive ability. In this study, we examined the effect of this direct selection on males on gene expression patterns in females. Differential gene expression was determined by whether a female was ancestral or evolved generation, indicating that gene expression changes were an evolved response due to indirect selection on females. Significantly differentially expressed genes were downregulated in evolved females. These genes tended to be female-biased in wildtype individuals and located on the X chromosome. The downregulation of X-linked genes suggests expression levels in females equal to or lower than that in males. Together these results indicate a less female-like transcriptome after experimental evolution. This supports a sexual conflict scenario by which direct sexual selection on males indirectly masculinizes the female transcriptome over short evolutionary timescales.},
}
RevDate: 2023-08-18
CmpDate: 2023-06-21
Comparative phylogenetic analysis and transcriptomic profiling of Dengue (DENV-3 genotype I) outbreak in 2021 in Bangladesh.
Virology journal, 20(1):127.
BACKGROUND: The next-generation sequencing (NGS) technology facilitates in-depth study of host-pathogen metatranscriptome. We, therefore, implicated phylodynamic and transcriptomic approaches through NGS technology to know/understand the dengue virus (DENV) origin and host response with dengue fever.
METHODS: In this study, blood serum RNA was extracted from 21 dengue patients and 3 healthy individuals. Total transcriptomic data were analyzed for phylogenetic, phylodynamic, differential express gene (DEG), and gene ontology (GO) using respective bioinformatics tools.
RESULTS: The viral genome sequence revealed dengue viral genome size ranges 10647 to 10707 nucleotide. Phylogenetic and phylodynamic analysis showed that the 2021 epidemic isolates were DENV-3 genotype-I and maintained as a new clade in compared to 2019 epidemic. Transcriptome analysis showed a total of 2686 genes were DEG in dengue patients compared to control with a q-value < 0.05. DESeq2 plot counts function of the top 24 genes with the smallest q-values of differential gene expression of RNA-seq data showed that 11 genes were upregulated, whereas 13 genes were downregulated. GO analysis showed a significant upregulation (p = < 0.001) in a process of multicellular organismal, nervous system, sensory perception of chemical stimulus, and G protein-coupled receptor signaling pathways in the dengue patients. However, there were a significant downregulation (p = < 0.001) of intracellular component, cellular anatomical entity, and protein-containing complex in dengue patients. Most importantly, there was a significant increase of a class of immunoregulatory proteins in dengue patients in compared to the controls, with increased GO of immune system process. In addition, upregulation of toll receptor (TLR) signaling pathways were found in dengue patients. These TLR pathways were particularly involved for the activation of innate system coupled with adaptive immune system that probably involved the rapid elimination of dengue virus infected cells. These differentially expressed genes could be further investigated for target based prophylactic interventions for dengue.
CONCLUSION: This is a first report describing DENV complete genomic features and differentially expressed genes in patients in Bangladesh. These genes may have diagnostic and therapeutic values for dengue infection. Continual genomic surveillance is required to further investigate the shift in dominant genotypes in relation to viral pathogenesis.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12985-023-02030-1.
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@article {pmid37337232,
year = {2023},
author = {Sarkar, MMH and Rahman, MS and Islam, MR and Rahman, A and Islam, MS and Banu, TA and Akter, S and Goswami, B and Jahan, I and Habib, MA and Uddin, MM and Mia, MZ and Miah, MI and Shaikh, AA and Khan, MS},
title = {Comparative phylogenetic analysis and transcriptomic profiling of Dengue (DENV-3 genotype I) outbreak in 2021 in Bangladesh.},
journal = {Virology journal},
volume = {20},
number = {1},
pages = {127},
pmid = {37337232},
issn = {1743-422X},
mesh = {Humans ; Phylogeny ; Bangladesh/epidemiology ; *Transcriptome ; *Dengue/epidemiology ; Disease Outbreaks ; Genotype ; Serogroup ; },
abstract = {BACKGROUND: The next-generation sequencing (NGS) technology facilitates in-depth study of host-pathogen metatranscriptome. We, therefore, implicated phylodynamic and transcriptomic approaches through NGS technology to know/understand the dengue virus (DENV) origin and host response with dengue fever.
METHODS: In this study, blood serum RNA was extracted from 21 dengue patients and 3 healthy individuals. Total transcriptomic data were analyzed for phylogenetic, phylodynamic, differential express gene (DEG), and gene ontology (GO) using respective bioinformatics tools.
RESULTS: The viral genome sequence revealed dengue viral genome size ranges 10647 to 10707 nucleotide. Phylogenetic and phylodynamic analysis showed that the 2021 epidemic isolates were DENV-3 genotype-I and maintained as a new clade in compared to 2019 epidemic. Transcriptome analysis showed a total of 2686 genes were DEG in dengue patients compared to control with a q-value < 0.05. DESeq2 plot counts function of the top 24 genes with the smallest q-values of differential gene expression of RNA-seq data showed that 11 genes were upregulated, whereas 13 genes were downregulated. GO analysis showed a significant upregulation (p = < 0.001) in a process of multicellular organismal, nervous system, sensory perception of chemical stimulus, and G protein-coupled receptor signaling pathways in the dengue patients. However, there were a significant downregulation (p = < 0.001) of intracellular component, cellular anatomical entity, and protein-containing complex in dengue patients. Most importantly, there was a significant increase of a class of immunoregulatory proteins in dengue patients in compared to the controls, with increased GO of immune system process. In addition, upregulation of toll receptor (TLR) signaling pathways were found in dengue patients. These TLR pathways were particularly involved for the activation of innate system coupled with adaptive immune system that probably involved the rapid elimination of dengue virus infected cells. These differentially expressed genes could be further investigated for target based prophylactic interventions for dengue.
CONCLUSION: This is a first report describing DENV complete genomic features and differentially expressed genes in patients in Bangladesh. These genes may have diagnostic and therapeutic values for dengue infection. Continual genomic surveillance is required to further investigate the shift in dominant genotypes in relation to viral pathogenesis.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12985-023-02030-1.},
}
MeSH Terms:
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Humans
Phylogeny
Bangladesh/epidemiology
*Transcriptome
*Dengue/epidemiology
Disease Outbreaks
Genotype
Serogroup
RevDate: 2023-08-17
Renaissance for magnetotactic bacteria in astrobiology.
The ISME journal [Epub ahead of print].
Capable of forming magnetofossils similar to some magnetite nanocrystals observed in the Martian meteorite ALH84001, magnetotactic bacteria (MTB) once occupied a special position in the field of astrobiology during the 1990s and 2000s. This flourish of interest in putative Martian magnetofossils faded from all but the experts studying magnetosome formation, based on claims that abiotic processes could produce magnetosome-like magnetite crystals. Recently, the rapid growth in our knowledge of the extreme environments in which MTB thrive and their phylogenic heritage, leads us to advocate for a renaissance of MTB in astrobiology. In recent decades, magnetotactic members have been discovered alive in natural extreme environments with wide ranges of salinity (up to 90 g L[-1]), pH (1-10), and temperature (0-70 °C). Additionally, some MTB populations are found to be able to survive irradiated, desiccated, metal-rich, hypomagnetic, or microgravity conditions, and are capable of utilizing simple inorganic compounds such as sulfate and nitrate. Moreover, MTB likely emerged quite early in Earth's history, coinciding with a period when the Martian surface was covered with liquid water as well as a strong magnetic field. MTB are commonly discovered in suboxic or oxic-anoxic interfaces in aquatic environments or sediments similar to ancient crater lakes on Mars, such as Gale crater and Jezero crater. Taken together, MTB can be exemplary model microorganisms in astrobiology research, and putative ancient Martian life, if it ever occurred, could plausibly have included magnetotactic microorganisms. Furthermore, we summarize multiple typical biosignatures that can be applied for the detection of ancient MTB on Earth and extraterrestrial MTB-like life. We suggest transporting MTB to space stations and simulation chambers to further investigate their tolerance potential and distinctive biosignatures to aid in understanding the evolutionary history of MTB and the potential of magnetofossils as an extraterrestrial biomarker.
Additional Links: PMID-37592065
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@article {pmid37592065,
year = {2023},
author = {Shen, J and Paterson, GA and Wang, Y and Kirschvink, JL and Pan, Y and Lin, W},
title = {Renaissance for magnetotactic bacteria in astrobiology.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
pmid = {37592065},
issn = {1751-7370},
support = {T2225011//National Natural Science Foundation of China (National Science Foundation of China)/ ; 42293293//National Natural Science Foundation of China (National Science Foundation of China)/ ; 42202339//National Natural Science Foundation of China (National Science Foundation of China)/ ; 2023M733478//China Postdoctoral Science Foundation/ ; NE/P017266/1//RCUK | Natural Environment Research Council (NERC)/ ; },
abstract = {Capable of forming magnetofossils similar to some magnetite nanocrystals observed in the Martian meteorite ALH84001, magnetotactic bacteria (MTB) once occupied a special position in the field of astrobiology during the 1990s and 2000s. This flourish of interest in putative Martian magnetofossils faded from all but the experts studying magnetosome formation, based on claims that abiotic processes could produce magnetosome-like magnetite crystals. Recently, the rapid growth in our knowledge of the extreme environments in which MTB thrive and their phylogenic heritage, leads us to advocate for a renaissance of MTB in astrobiology. In recent decades, magnetotactic members have been discovered alive in natural extreme environments with wide ranges of salinity (up to 90 g L[-1]), pH (1-10), and temperature (0-70 °C). Additionally, some MTB populations are found to be able to survive irradiated, desiccated, metal-rich, hypomagnetic, or microgravity conditions, and are capable of utilizing simple inorganic compounds such as sulfate and nitrate. Moreover, MTB likely emerged quite early in Earth's history, coinciding with a period when the Martian surface was covered with liquid water as well as a strong magnetic field. MTB are commonly discovered in suboxic or oxic-anoxic interfaces in aquatic environments or sediments similar to ancient crater lakes on Mars, such as Gale crater and Jezero crater. Taken together, MTB can be exemplary model microorganisms in astrobiology research, and putative ancient Martian life, if it ever occurred, could plausibly have included magnetotactic microorganisms. Furthermore, we summarize multiple typical biosignatures that can be applied for the detection of ancient MTB on Earth and extraterrestrial MTB-like life. We suggest transporting MTB to space stations and simulation chambers to further investigate their tolerance potential and distinctive biosignatures to aid in understanding the evolutionary history of MTB and the potential of magnetofossils as an extraterrestrial biomarker.},
}
RevDate: 2023-08-17
Advances in oral mesenchymal stem cell-derived extracellular vesicles in health and disease.
Genes & diseases, 11(1):346-357.
Extracellular vesicles (EVs) are nano-size vesicles secreted naturally by all cells into the extracellular space and have been recognized as important cell-cell mediators in multicellular organisms. EVs contain nucleic acids, proteins, lipids, and other cellular components, regulating many basic biological processes and playing an important role in regenerative medicine and diseases. EVs can be traced to their cells of origin and exhibit a similar function. Moreover, EVs demonstrate low immunogenicity, good biocompatibility, and fewer side effects, compared to their parent cells. Mesenchymal stem cells (MSCs) are one of the most important resource cells for EVs, with a great capacity for self-renewal and multipotent differentiation, and play an essential role in stem cell therapy. The mechanism of MSC therapy was thought to be attributed to the differentiation of MSCs after targeted migration, as previously noted. However, emerging evidence shows the previously unknown role of MSC-derived paracrine factors in stem cell therapy. Especially EVs derived from oral tissue MSCs (OMSC-EVs), show more advantages than those of all other MSCs in tissue repair and regeneration, due to their lower invasiveness and easier accessibility for sample collection. Here, we systematically review the biogenesis and biological characteristics of OMSC-EVs, as well as the role of OMSC-EVs in intercellular communication. Furthermore, we discuss the potential therapeutic roles of OMSC-EVs in oral and systemic diseases. We highlight the current challenges and future directions of OMSC-EVs to focus more attention on clinical translation. We aim to provide valuable insights for the explorative clinical application of OMSC-EVs.
Additional Links: PMID-37588220
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Citation:
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@article {pmid37588220,
year = {2024},
author = {Luo, H and Birjandi, AA and Ren, F and Sun, T and Sharpe, PT and Sun, H and An, Z},
title = {Advances in oral mesenchymal stem cell-derived extracellular vesicles in health and disease.},
journal = {Genes & diseases},
volume = {11},
number = {1},
pages = {346-357},
pmid = {37588220},
issn = {2352-3042},
abstract = {Extracellular vesicles (EVs) are nano-size vesicles secreted naturally by all cells into the extracellular space and have been recognized as important cell-cell mediators in multicellular organisms. EVs contain nucleic acids, proteins, lipids, and other cellular components, regulating many basic biological processes and playing an important role in regenerative medicine and diseases. EVs can be traced to their cells of origin and exhibit a similar function. Moreover, EVs demonstrate low immunogenicity, good biocompatibility, and fewer side effects, compared to their parent cells. Mesenchymal stem cells (MSCs) are one of the most important resource cells for EVs, with a great capacity for self-renewal and multipotent differentiation, and play an essential role in stem cell therapy. The mechanism of MSC therapy was thought to be attributed to the differentiation of MSCs after targeted migration, as previously noted. However, emerging evidence shows the previously unknown role of MSC-derived paracrine factors in stem cell therapy. Especially EVs derived from oral tissue MSCs (OMSC-EVs), show more advantages than those of all other MSCs in tissue repair and regeneration, due to their lower invasiveness and easier accessibility for sample collection. Here, we systematically review the biogenesis and biological characteristics of OMSC-EVs, as well as the role of OMSC-EVs in intercellular communication. Furthermore, we discuss the potential therapeutic roles of OMSC-EVs in oral and systemic diseases. We highlight the current challenges and future directions of OMSC-EVs to focus more attention on clinical translation. We aim to provide valuable insights for the explorative clinical application of OMSC-EVs.},
}
RevDate: 2023-08-16
Replaying the evolution of multicellularity.
Trends in ecology & evolution pii:S0169-5347(23)00209-4 [Epub ahead of print].
The first organisms on Earth were presumably unicellular. At one point, evolution shaped these individual cells into multicellular organisms, which was a significant transition in the history of life on Earth. To investigate how this change happened, Bozdag et al. re-ran evolution in the lab and observed how single-celled yeast forms large multicellular aggregates.
Additional Links: PMID-37586948
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PubMed:
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@article {pmid37586948,
year = {2023},
author = {Shalev, O and Ye, X and Ratzke, C},
title = {Replaying the evolution of multicellularity.},
journal = {Trends in ecology & evolution},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tree.2023.07.007},
pmid = {37586948},
issn = {1872-8383},
abstract = {The first organisms on Earth were presumably unicellular. At one point, evolution shaped these individual cells into multicellular organisms, which was a significant transition in the history of life on Earth. To investigate how this change happened, Bozdag et al. re-ran evolution in the lab and observed how single-celled yeast forms large multicellular aggregates.},
}
RevDate: 2023-08-11
Strong purifying selection in haploid tissue-specific genes of Scots pine supports the masking theory.
Molecular biology and evolution pii:7241103 [Epub ahead of print].
The masking theory states that genes expressed in haploid stage will be under more efficient selection. In contrast, selection will be less efficient in genes expressed in diploid stage, where the fitness effects of recessive deleterious or beneficial mutations can be hidden from selection in heterozygous form. This difference can influence several evolutionary processes such as the maintenance of genetic variation, adaptation rate, and genetic load. Masking theory expectations have been confirmed in single-cell haploid and diploid organisms. However, in multicellular organisms, such as plants, the effects of haploid selection are not clear-cut. In plants, the great majority of studies indicating haploid selection have been carried out using male haploid tissues in angiosperms. Hence, evidence in these systems is confounded with the effects of sexual selection and intra-specific competition. Evidence from other plant groups is scarce and results show no support for the masking theory. Here we have used a gymnosperm Scots pine megagametophyte, a maternally-derived seed haploid tissue, and four diploid tissues to test the strength of purifying selection on a set of genes with tissue-specific expression. By using targeted resequencing data of those genes, we obtained estimates of genetic diversity, the site frequency spectrum of 0-fold and 4-fold sites, and inferred the distribution of fitness effects (DFE) of new mutations in haploid and diploid tissue-specific genes. Our results show that purifying selection is stronger for tissue-specific genes expressed in the haploid megagametophyte tissue, and that this signal of strong selection is not an artifact driven by high expression levels.
Additional Links: PMID-37565532
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@article {pmid37565532,
year = {2023},
author = {Cervantes, S and Kesälahti, R and Kumpula, TA and Mattila, TM and Helanterä, H and Pyhäjärvi, T},
title = {Strong purifying selection in haploid tissue-specific genes of Scots pine supports the masking theory.},
journal = {Molecular biology and evolution},
volume = {},
number = {},
pages = {},
doi = {10.1093/molbev/msad183},
pmid = {37565532},
issn = {1537-1719},
abstract = {The masking theory states that genes expressed in haploid stage will be under more efficient selection. In contrast, selection will be less efficient in genes expressed in diploid stage, where the fitness effects of recessive deleterious or beneficial mutations can be hidden from selection in heterozygous form. This difference can influence several evolutionary processes such as the maintenance of genetic variation, adaptation rate, and genetic load. Masking theory expectations have been confirmed in single-cell haploid and diploid organisms. However, in multicellular organisms, such as plants, the effects of haploid selection are not clear-cut. In plants, the great majority of studies indicating haploid selection have been carried out using male haploid tissues in angiosperms. Hence, evidence in these systems is confounded with the effects of sexual selection and intra-specific competition. Evidence from other plant groups is scarce and results show no support for the masking theory. Here we have used a gymnosperm Scots pine megagametophyte, a maternally-derived seed haploid tissue, and four diploid tissues to test the strength of purifying selection on a set of genes with tissue-specific expression. By using targeted resequencing data of those genes, we obtained estimates of genetic diversity, the site frequency spectrum of 0-fold and 4-fold sites, and inferred the distribution of fitness effects (DFE) of new mutations in haploid and diploid tissue-specific genes. Our results show that purifying selection is stronger for tissue-specific genes expressed in the haploid megagametophyte tissue, and that this signal of strong selection is not an artifact driven by high expression levels.},
}
RevDate: 2023-08-10
Programmed Necrosis in Host Defense.
Current topics in microbiology and immunology [Epub ahead of print].
Host control over infectious disease relies on the ability of cells in multicellular organisms to detect and defend against pathogens to prevent disease. Evolution affords mammals with a wide variety of independent immune mechanisms to control or eliminate invading infectious agents. Many pathogens acquire functions to deflect these immune mechanisms and promote infection. Following successful invasion of a host, cell autonomous signaling pathways drive the production of inflammatory cytokines, deployment of restriction factors and induction of cell death. Combined, these innate immune mechanisms attract dendritic cells, neutrophils and macrophages as well as innate lymphoid cells such as natural killer cells that all help control infection. Eventually, the development of adaptive pathogen-specific immunity clears infection and provides immune memory of the encounter. For obligate intracellular pathogens such as viruses, diverse cell death pathways make a pivotal contribution to early control by eliminating host cells before progeny are produced. Pro-apoptotic caspase-8 activity (along with caspase-10 in humans) executes extrinsic apoptosis, a nonlytic form of cell death triggered by TNF family death receptors (DRs). Over the past two decades, alternate extrinsic apoptosis and necroptosis outcomes have been described. Programmed necrosis, or necroptosis, occurs when receptor interacting protein kinase 3 (RIPK3) activates mixed lineage kinase-like (MLKL), causing cell leakage. Thus, activation of DRs, toll-like receptors (TLRs) or pathogen sensor Z-nucleic acid binding protein 1 (ZBP1) initiates apoptosis as well as necroptosis if not blocked by virus-encoded inhibitors. Mammalian cell death pathways are blocked by herpesvirus- and poxvirus-encoded cell death suppressors. Growing evidence has revealed the importance of Z-nucleic acid sensor, ZBP1, in the cell autonomous recognition of both DNA and RNA virus infection. This volume will explore the detente between viruses and cells to manage death machinery and avoid elimination to support dissemination within the host animal.
Additional Links: PMID-37563336
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PubMed:
Citation:
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@article {pmid37563336,
year = {2023},
author = {Mocarski, ES},
title = {Programmed Necrosis in Host Defense.},
journal = {Current topics in microbiology and immunology},
volume = {},
number = {},
pages = {},
doi = {10.1007/82_2023_264},
pmid = {37563336},
issn = {0070-217X},
abstract = {Host control over infectious disease relies on the ability of cells in multicellular organisms to detect and defend against pathogens to prevent disease. Evolution affords mammals with a wide variety of independent immune mechanisms to control or eliminate invading infectious agents. Many pathogens acquire functions to deflect these immune mechanisms and promote infection. Following successful invasion of a host, cell autonomous signaling pathways drive the production of inflammatory cytokines, deployment of restriction factors and induction of cell death. Combined, these innate immune mechanisms attract dendritic cells, neutrophils and macrophages as well as innate lymphoid cells such as natural killer cells that all help control infection. Eventually, the development of adaptive pathogen-specific immunity clears infection and provides immune memory of the encounter. For obligate intracellular pathogens such as viruses, diverse cell death pathways make a pivotal contribution to early control by eliminating host cells before progeny are produced. Pro-apoptotic caspase-8 activity (along with caspase-10 in humans) executes extrinsic apoptosis, a nonlytic form of cell death triggered by TNF family death receptors (DRs). Over the past two decades, alternate extrinsic apoptosis and necroptosis outcomes have been described. Programmed necrosis, or necroptosis, occurs when receptor interacting protein kinase 3 (RIPK3) activates mixed lineage kinase-like (MLKL), causing cell leakage. Thus, activation of DRs, toll-like receptors (TLRs) or pathogen sensor Z-nucleic acid binding protein 1 (ZBP1) initiates apoptosis as well as necroptosis if not blocked by virus-encoded inhibitors. Mammalian cell death pathways are blocked by herpesvirus- and poxvirus-encoded cell death suppressors. Growing evidence has revealed the importance of Z-nucleic acid sensor, ZBP1, in the cell autonomous recognition of both DNA and RNA virus infection. This volume will explore the detente between viruses and cells to manage death machinery and avoid elimination to support dissemination within the host animal.},
}
RevDate: 2023-08-10
Transcriptome analyses of leaf architecture in Sansevieria support a common genetic toolkit in the parallel evolution of unifacial leaves in monocots.
Plant direct, 7(8):e511.
Planar structures dramatically increase the surface-area-to-volume ratio, which is critically important for multicellular organisms. In this study, we utilize naturally occurring phenotypic variation among three Sansivieria species (Asperagaceae) to investigate leaf margin expression patterns that are associated with mediolateral and adaxial/abaxial development. We identified differentially expressed genes (DEGs) between center and margin leaf tissues in two planar-leaf species Sansevieria subspicata and Sansevieria trifasciata and compared these with expression patterns within the cylindrically leaved Sansevieria cylindrica. Two YABBY family genes, homologs of FILAMENTOUS FLOWER and DROOPING LEAF, are overexpressed in the center leaf tissue in the planar-leaf species and in the tissue of the cylindrical leaves. As mesophyll structure does not indicate adaxial versus abaxial differentiation, increased leaf thickness results in more water-storage tissue and enhances resistance to aridity. This suggests that the cylindrical-leaf in S. cylindrica is analogous to the central leaf tissue in the planar-leaf species. Furthermore, the congruence of the expression patterns of these YABBY genes in Sansevieria with expression patterns found in other unifacial monocot species suggests that patterns of parallel evolution may be the result of similar solutions derived from a limited developmental toolbox.
Additional Links: PMID-37559824
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@article {pmid37559824,
year = {2023},
author = {Golenberg, EM and Popadić, A and Hao, W},
title = {Transcriptome analyses of leaf architecture in Sansevieria support a common genetic toolkit in the parallel evolution of unifacial leaves in monocots.},
journal = {Plant direct},
volume = {7},
number = {8},
pages = {e511},
pmid = {37559824},
issn = {2475-4455},
abstract = {Planar structures dramatically increase the surface-area-to-volume ratio, which is critically important for multicellular organisms. In this study, we utilize naturally occurring phenotypic variation among three Sansivieria species (Asperagaceae) to investigate leaf margin expression patterns that are associated with mediolateral and adaxial/abaxial development. We identified differentially expressed genes (DEGs) between center and margin leaf tissues in two planar-leaf species Sansevieria subspicata and Sansevieria trifasciata and compared these with expression patterns within the cylindrically leaved Sansevieria cylindrica. Two YABBY family genes, homologs of FILAMENTOUS FLOWER and DROOPING LEAF, are overexpressed in the center leaf tissue in the planar-leaf species and in the tissue of the cylindrical leaves. As mesophyll structure does not indicate adaxial versus abaxial differentiation, increased leaf thickness results in more water-storage tissue and enhances resistance to aridity. This suggests that the cylindrical-leaf in S. cylindrica is analogous to the central leaf tissue in the planar-leaf species. Furthermore, the congruence of the expression patterns of these YABBY genes in Sansevieria with expression patterns found in other unifacial monocot species suggests that patterns of parallel evolution may be the result of similar solutions derived from a limited developmental toolbox.},
}
RevDate: 2023-08-09
Developmental selection and the perception of mutation bias.
Molecular biology and evolution pii:7240090 [Epub ahead of print].
The notion that mutations are random relative to their fitness effects is central to the Neo-Darwinian view of evolution. However, a recent interpretation of the patterns of mutation accumulation in the genome of Arabidopsis thaliana has challenged this notion, arguing for the presence of a targeted DNA repair mechanism that causes a non-random association of mutation rates and fitness effects. Specifically, this mechanism was suggested to cause a reduction in the rates of mutations on essential genes, thus lowering the rates of deleterious mutations. Central to this argument were attempts to rule out selection at the population level. Here, we offer an alternative and parsimonious interpretation of the patterns of mutation accumulation previously attributed to mutation bias, showing how they can instead or additionally be caused by developmental selection, i.e., selection occurring at the cellular level during the development of a multicellular organism. Thus, the depletion of deleterious mutations in A. thaliana may indeed be the result of a selective process, rather than a bias in mutation. More broadly, our work highlights the importance of considering development in the interpretation of population genetic analyses of multicellular organisms, and it emphasizes that efforts to identify mechanisms involved in mutational biases should explicitly account for developmental selection.
Additional Links: PMID-37556606
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@article {pmid37556606,
year = {2023},
author = {Majic, P and Payne, JL},
title = {Developmental selection and the perception of mutation bias.},
journal = {Molecular biology and evolution},
volume = {},
number = {},
pages = {},
doi = {10.1093/molbev/msad179},
pmid = {37556606},
issn = {1537-1719},
abstract = {The notion that mutations are random relative to their fitness effects is central to the Neo-Darwinian view of evolution. However, a recent interpretation of the patterns of mutation accumulation in the genome of Arabidopsis thaliana has challenged this notion, arguing for the presence of a targeted DNA repair mechanism that causes a non-random association of mutation rates and fitness effects. Specifically, this mechanism was suggested to cause a reduction in the rates of mutations on essential genes, thus lowering the rates of deleterious mutations. Central to this argument were attempts to rule out selection at the population level. Here, we offer an alternative and parsimonious interpretation of the patterns of mutation accumulation previously attributed to mutation bias, showing how they can instead or additionally be caused by developmental selection, i.e., selection occurring at the cellular level during the development of a multicellular organism. Thus, the depletion of deleterious mutations in A. thaliana may indeed be the result of a selective process, rather than a bias in mutation. More broadly, our work highlights the importance of considering development in the interpretation of population genetic analyses of multicellular organisms, and it emphasizes that efforts to identify mechanisms involved in mutational biases should explicitly account for developmental selection.},
}
RevDate: 2023-08-08
Single and two-cells shape analysis from energy functionals for three-dimensional vertex models.
International journal for numerical methods in biomedical engineering [Epub ahead of print].
Vertex models have been extensively used for simulating the evolution of multicellular systems, and have given rise to important global properties concerning their macroscopic rheology or jamming transitions. These models are based on the definition of an energy functional, which fully determines the cellular response and conclusions. While two-dimensional vertex models have been widely employed, three-dimensional models are far more scarce, mainly due to the large amount of configurations that they may adopt and the complex geometrical transitions they undergo. We here investigate the shape of single and two-cells configurations as a function of the energy terms, and we study the dependence of the final shape on the model parameters: namely the exponent of the term penalising cell-cell adhesion and surface contractility. In single cell analysis, we deduce analytically the radius and limit values of the contractility for linear and quadratic surface energy terms, in 2D and 3D. In two-cells systems, symmetrical and asymmetrical, we deduce the evolution of the aspect ratio and the relative radius. While in functionals with linear surface terms yield the same aspect ratio in 2D and 3D, the configurations when using quadratic surface terms are distinct. We relate our results with well-known solutions from capillarity theory, and verify our analytical findings with a three-dimensional vertex model.
Additional Links: PMID-37551449
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@article {pmid37551449,
year = {2023},
author = {Khan, AK and Muñoz-Castro, G and Muñoz, JJ},
title = {Single and two-cells shape analysis from energy functionals for three-dimensional vertex models.},
journal = {International journal for numerical methods in biomedical engineering},
volume = {},
number = {},
pages = {e3766},
doi = {10.1002/cnm.3766},
pmid = {37551449},
issn = {2040-7947},
support = {//Generalitat de Catalunya/ ; //Ministerio de Ciencia e Innovación/ ; //Ministry of Federal Education and Professional Training/ ; //Higher Education Commission (under the Ministry of Federal Education and Professional Training) of Pakistan/ ; CEX2018-000797-S//Spanish Ministry of Science and Innovation/ ; PID2020-116141GB-I00//Spanish Ministry of Science and Innovation/ ; 2021 SGR 01049//Catalan government Generalitat de Catalunya/ ; },
abstract = {Vertex models have been extensively used for simulating the evolution of multicellular systems, and have given rise to important global properties concerning their macroscopic rheology or jamming transitions. These models are based on the definition of an energy functional, which fully determines the cellular response and conclusions. While two-dimensional vertex models have been widely employed, three-dimensional models are far more scarce, mainly due to the large amount of configurations that they may adopt and the complex geometrical transitions they undergo. We here investigate the shape of single and two-cells configurations as a function of the energy terms, and we study the dependence of the final shape on the model parameters: namely the exponent of the term penalising cell-cell adhesion and surface contractility. In single cell analysis, we deduce analytically the radius and limit values of the contractility for linear and quadratic surface energy terms, in 2D and 3D. In two-cells systems, symmetrical and asymmetrical, we deduce the evolution of the aspect ratio and the relative radius. While in functionals with linear surface terms yield the same aspect ratio in 2D and 3D, the configurations when using quadratic surface terms are distinct. We relate our results with well-known solutions from capillarity theory, and verify our analytical findings with a three-dimensional vertex model.},
}
RevDate: 2023-08-07
The Hippo kinase cascade regulates a contractile cell behavior and cell density in a close unicellular relative of animals.
bioRxiv : the preprint server for biology pii:2023.07.25.550562.
The genomes of close unicellular relatives of animals encode orthologs of many genes that regulate animal development. However, little is known about the function of such genes in unicellular organisms or the evolutionary process by which these genes came to function in multicellular development. The Hippo pathway, which regulates cell proliferation and tissue size in animals, is present in some of the closest unicellular relatives of animals, including the amoeboid organism Capsaspora owczarzaki . We previously showed that the Capsaspora ortholog of the Hippo pathway nuclear effector Yorkie/YAP/TAZ (coYki) regulates actin dynamics and the three-dimensional morphology of Capsaspora cell aggregates, but is dispensable for cell proliferation control (Phillips et al., 2022). However, the function of upstream Hippo pathway components, and whether and how they regulate coYki in Capsaspora , remained unknown. Here, we analyze the function of the upstream Hippo pathway kinases coHpo and coWts in Capsaspora by generating mutant lines for each gene. Loss of either kinase results in increased nuclear localization of coYki, indicating an ancient, premetazoan origin of this Hippo pathway regulatory mechanism. Strikingly, we find that loss of either kinase causes a contractile cell behavior and increased density of cell packing within Capsaspora aggregates. We further show that this increased cell density is not due to differences in proliferation, but rather actomyosin-dependent changes in the multicellular architecture of aggregates. Given its well-established role in cell density-regulated proliferation in animals, the increased density of cell packing in coHpo and coWts mutants suggests a shared and possibly ancient and conserved function of the Hippo pathway in cell density control. Together, these results implicate cytoskeletal regulation but not proliferation as an ancestral function of the Hippo pathway and uncover a novel role for Hippo signaling in regulating cell density in a proliferation-independent manner.
Additional Links: PMID-37546755
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@article {pmid37546755,
year = {2023},
author = {Phillips, JE and Pan, D},
title = {The Hippo kinase cascade regulates a contractile cell behavior and cell density in a close unicellular relative of animals.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2023.07.25.550562},
pmid = {37546755},
abstract = {The genomes of close unicellular relatives of animals encode orthologs of many genes that regulate animal development. However, little is known about the function of such genes in unicellular organisms or the evolutionary process by which these genes came to function in multicellular development. The Hippo pathway, which regulates cell proliferation and tissue size in animals, is present in some of the closest unicellular relatives of animals, including the amoeboid organism Capsaspora owczarzaki . We previously showed that the Capsaspora ortholog of the Hippo pathway nuclear effector Yorkie/YAP/TAZ (coYki) regulates actin dynamics and the three-dimensional morphology of Capsaspora cell aggregates, but is dispensable for cell proliferation control (Phillips et al., 2022). However, the function of upstream Hippo pathway components, and whether and how they regulate coYki in Capsaspora , remained unknown. Here, we analyze the function of the upstream Hippo pathway kinases coHpo and coWts in Capsaspora by generating mutant lines for each gene. Loss of either kinase results in increased nuclear localization of coYki, indicating an ancient, premetazoan origin of this Hippo pathway regulatory mechanism. Strikingly, we find that loss of either kinase causes a contractile cell behavior and increased density of cell packing within Capsaspora aggregates. We further show that this increased cell density is not due to differences in proliferation, but rather actomyosin-dependent changes in the multicellular architecture of aggregates. Given its well-established role in cell density-regulated proliferation in animals, the increased density of cell packing in coHpo and coWts mutants suggests a shared and possibly ancient and conserved function of the Hippo pathway in cell density control. Together, these results implicate cytoskeletal regulation but not proliferation as an ancestral function of the Hippo pathway and uncover a novel role for Hippo signaling in regulating cell density in a proliferation-independent manner.},
}
RevDate: 2023-08-07
CmpDate: 2023-08-07
The circadian clock of the bacterium B. subtilis evokes properties of complex, multicellular circadian systems.
Science advances, 9(31):eadh1308.
Circadian clocks are pervasive throughout nature, yet only recently has this adaptive regulatory program been described in nonphotosynthetic bacteria. Here, we describe an inherent complexity in the Bacillus subtilis circadian clock. We find that B. subtilis entrains to blue and red light and that circadian entrainment is separable from masking through fluence titration and frequency demultiplication protocols. We identify circadian rhythmicity in constant light, consistent with the Aschoff's rule, and entrainment aftereffects, both of which are properties described for eukaryotic circadian clocks. We report that circadian rhythms occur in wild isolates of this prokaryote, thus establishing them as a general property of this species, and that its circadian system responds to the environment in a complex fashion that is consistent with multicellular eukaryotic circadian systems.
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@article {pmid37540742,
year = {2023},
author = {Sartor, F and Xu, X and Popp, T and Dodd, AN and Kovács, ÁT and Merrow, M},
title = {The circadian clock of the bacterium B. subtilis evokes properties of complex, multicellular circadian systems.},
journal = {Science advances},
volume = {9},
number = {31},
pages = {eadh1308},
pmid = {37540742},
issn = {2375-2548},
mesh = {*Circadian Clocks ; Bacillus subtilis ; Circadian Rhythm ; Light ; Eukaryota ; },
abstract = {Circadian clocks are pervasive throughout nature, yet only recently has this adaptive regulatory program been described in nonphotosynthetic bacteria. Here, we describe an inherent complexity in the Bacillus subtilis circadian clock. We find that B. subtilis entrains to blue and red light and that circadian entrainment is separable from masking through fluence titration and frequency demultiplication protocols. We identify circadian rhythmicity in constant light, consistent with the Aschoff's rule, and entrainment aftereffects, both of which are properties described for eukaryotic circadian clocks. We report that circadian rhythms occur in wild isolates of this prokaryote, thus establishing them as a general property of this species, and that its circadian system responds to the environment in a complex fashion that is consistent with multicellular eukaryotic circadian systems.},
}
MeSH Terms:
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*Circadian Clocks
Bacillus subtilis
Circadian Rhythm
Light
Eukaryota
RevDate: 2023-08-01
CmpDate: 2023-07-31
The Price of Human Evolution: Cancer-Testis Antigens, the Decline in Male Fertility and the Increase in Cancer.
International journal of molecular sciences, 24(14):.
The increasing frequency of general and particularly male cancer coupled with the reduction in male fertility seen worldwide motivated us to seek a potential evolutionary link between these two phenomena, concerning the reproductive transcriptional modules observed in cancer and the expression of cancer-testis antigens (CTA). The phylostratigraphy analysis of the human genome allowed us to link the early evolutionary origin of cancer via the reproductive life cycles of the unicellulars and early multicellulars, potentially driving soma-germ transition, female meiosis, and the parthenogenesis of polyploid giant cancer cells (PGCCs), with the expansion of the CTA multi-families, very late during their evolution. CTA adaptation was aided by retrovirus domestication in the unstable genomes of mammals, for protecting male fertility in stress conditions, particularly that of humans, as compensation for the energy consumption of a large complex brain which also exploited retrotransposition. We found that the early and late evolutionary branches of human cancer are united by the immunity-proto-placental network, which evolved in the Cambrian and shares stress regulators with the finely-tuned sex determination system. We further propose that social stress and endocrine disruption caused by environmental pollution with organic materials, which alter sex determination in male foetuses and further spermatogenesis in adults, bias the development of PGCC-parthenogenetic cancer by default.
Additional Links: PMID-37511419
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@article {pmid37511419,
year = {2023},
author = {Erenpreisa, J and Vainshelbaum, NM and Lazovska, M and Karklins, R and Salmina, K and Zayakin, P and Rumnieks, F and Inashkina, I and Pjanova, D and Erenpreiss, J},
title = {The Price of Human Evolution: Cancer-Testis Antigens, the Decline in Male Fertility and the Increase in Cancer.},
journal = {International journal of molecular sciences},
volume = {24},
number = {14},
pages = {},
pmid = {37511419},
issn = {1422-0067},
mesh = {Pregnancy ; Animals ; Humans ; Male ; Female ; *Testis/metabolism ; Placenta ; Spermatogenesis/genetics ; Reproduction ; *Neoplasms/genetics/metabolism ; Mammals ; Polyploidy ; Fertility/genetics ; },
abstract = {The increasing frequency of general and particularly male cancer coupled with the reduction in male fertility seen worldwide motivated us to seek a potential evolutionary link between these two phenomena, concerning the reproductive transcriptional modules observed in cancer and the expression of cancer-testis antigens (CTA). The phylostratigraphy analysis of the human genome allowed us to link the early evolutionary origin of cancer via the reproductive life cycles of the unicellulars and early multicellulars, potentially driving soma-germ transition, female meiosis, and the parthenogenesis of polyploid giant cancer cells (PGCCs), with the expansion of the CTA multi-families, very late during their evolution. CTA adaptation was aided by retrovirus domestication in the unstable genomes of mammals, for protecting male fertility in stress conditions, particularly that of humans, as compensation for the energy consumption of a large complex brain which also exploited retrotransposition. We found that the early and late evolutionary branches of human cancer are united by the immunity-proto-placental network, which evolved in the Cambrian and shares stress regulators with the finely-tuned sex determination system. We further propose that social stress and endocrine disruption caused by environmental pollution with organic materials, which alter sex determination in male foetuses and further spermatogenesis in adults, bias the development of PGCC-parthenogenetic cancer by default.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Pregnancy
Animals
Humans
Male
Female
*Testis/metabolism
Placenta
Spermatogenesis/genetics
Reproduction
*Neoplasms/genetics/metabolism
Mammals
Polyploidy
Fertility/genetics
RevDate: 2023-07-27
A reinvestigation of multiple independent evolution and Triassic-Jurassic origin of multicellular Volvocine algae.
Genome biology and evolution pii:7232264 [Epub ahead of print].
The evolution of multicellular organisms is considered to be a major evolutionary transition, profoundly affecting the ecology and evolution of nearly all life on earth. The volvocine algae, a unique clade of chlorophytes with diverse cell morphology, provide an appealing model for investigating the evolution of multicellularity and development. However, the phylogenetic relationship and timescale of the volvocine algae are not fully resolved. Here, we use extensive taxon and gene sampling to reconstruct the phylogeny of the volvocine algae. Our results support that the colonial volvocine algae are not monophyletic group, and multicellularity independently evolve at least twice in the volvocine algae, once in Tetrabaenaceae and another in the Goniaceae + Volvocaceae. The simulation analyses suggest that incomplete lineage sorting is a major factor for the tree topology discrepancy, which imply that the multispecies coalescent model better fits the data used in this study. The coalescent-based species tree supports that the Goniaceae is monophyletic, and Crucicarteria is the earliest diverging lineage, followed by Hafniomonas and Radicarteria within the Volvocales. By considering the multiple uncertainties in divergence time estimation, the dating analyses indicate that the volvocine algae occurred during the Cryogenian to Ediacaran (696.6-551.1 Ma), and multicellularity in the volvocine algae originated from the Triassic to Jurassic. Our phylogeny and timeline provide an evolutionary framework for studying the evolution of key traits and the origin of multicellularity in the volvocine algae.
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@article {pmid37498572,
year = {2023},
author = {Ma, X and Shi, X and Wang, Q and Zhao, M and Zhang, Z and Zhong, B},
title = {A reinvestigation of multiple independent evolution and Triassic-Jurassic origin of multicellular Volvocine algae.},
journal = {Genome biology and evolution},
volume = {},
number = {},
pages = {},
doi = {10.1093/gbe/evad142},
pmid = {37498572},
issn = {1759-6653},
abstract = {The evolution of multicellular organisms is considered to be a major evolutionary transition, profoundly affecting the ecology and evolution of nearly all life on earth. The volvocine algae, a unique clade of chlorophytes with diverse cell morphology, provide an appealing model for investigating the evolution of multicellularity and development. However, the phylogenetic relationship and timescale of the volvocine algae are not fully resolved. Here, we use extensive taxon and gene sampling to reconstruct the phylogeny of the volvocine algae. Our results support that the colonial volvocine algae are not monophyletic group, and multicellularity independently evolve at least twice in the volvocine algae, once in Tetrabaenaceae and another in the Goniaceae + Volvocaceae. The simulation analyses suggest that incomplete lineage sorting is a major factor for the tree topology discrepancy, which imply that the multispecies coalescent model better fits the data used in this study. The coalescent-based species tree supports that the Goniaceae is monophyletic, and Crucicarteria is the earliest diverging lineage, followed by Hafniomonas and Radicarteria within the Volvocales. By considering the multiple uncertainties in divergence time estimation, the dating analyses indicate that the volvocine algae occurred during the Cryogenian to Ediacaran (696.6-551.1 Ma), and multicellularity in the volvocine algae originated from the Triassic to Jurassic. Our phylogeny and timeline provide an evolutionary framework for studying the evolution of key traits and the origin of multicellularity in the volvocine algae.},
}
RevDate: 2023-08-07
CmpDate: 2023-07-28
ROS are evolutionary conserved cell-to-cell stress signals.
Proceedings of the National Academy of Sciences of the United States of America, 120(31):e2305496120.
Cell-to-cell communication is fundamental to multicellular organisms and unicellular organisms living in a microbiome. It is thought to have evolved as a stress- or quorum-sensing mechanism in unicellular organisms. A unique cell-to-cell communication mechanism that uses reactive oxygen species (ROS) as a signal (termed the "ROS wave") was identified in flowering plants. This process is essential for systemic signaling and plant acclimation to stress and can spread from a small group of cells to the entire plant within minutes. Whether a similar signaling process is found in other organisms is however unknown. Here, we report that the ROS wave can be found in unicellular algae, amoeba, ferns, mosses, mammalian cells, and isolated hearts. We further show that this process can be triggered in unicellular and multicellular organisms by a local stress or H2O2 treatment and blocked by the application of catalase or NADPH oxidase inhibitors and that in unicellular algae it communicates important stress-response signals between cells. Taken together, our findings suggest that an active process of cell-to-cell ROS signaling, like the ROS wave, evolved before unicellular and multicellular organisms diverged. This mechanism could have communicated an environmental stress signal between cells and coordinated the acclimation response of many different cells living in a community. The finding of a signaling process, like the ROS wave, in mammalian cells further contributes to our understanding of different diseases and could impact the development of drugs that target for example cancer or heart disease.
Additional Links: PMID-37494396
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@article {pmid37494396,
year = {2023},
author = {Fichman, Y and Rowland, L and Oliver, MJ and Mittler, R},
title = {ROS are evolutionary conserved cell-to-cell stress signals.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {120},
number = {31},
pages = {e2305496120},
pmid = {37494396},
issn = {1091-6490},
support = {R01 GM111364/GM/NIGMS NIH HHS/United States ; GM111364/GM/NIGMS NIH HHS/United States ; },
mesh = {Animals ; Reactive Oxygen Species ; *Hydrogen Peroxide ; *Signal Transduction ; Cell Communication ; Plants ; Mammals ; },
abstract = {Cell-to-cell communication is fundamental to multicellular organisms and unicellular organisms living in a microbiome. It is thought to have evolved as a stress- or quorum-sensing mechanism in unicellular organisms. A unique cell-to-cell communication mechanism that uses reactive oxygen species (ROS) as a signal (termed the "ROS wave") was identified in flowering plants. This process is essential for systemic signaling and plant acclimation to stress and can spread from a small group of cells to the entire plant within minutes. Whether a similar signaling process is found in other organisms is however unknown. Here, we report that the ROS wave can be found in unicellular algae, amoeba, ferns, mosses, mammalian cells, and isolated hearts. We further show that this process can be triggered in unicellular and multicellular organisms by a local stress or H2O2 treatment and blocked by the application of catalase or NADPH oxidase inhibitors and that in unicellular algae it communicates important stress-response signals between cells. Taken together, our findings suggest that an active process of cell-to-cell ROS signaling, like the ROS wave, evolved before unicellular and multicellular organisms diverged. This mechanism could have communicated an environmental stress signal between cells and coordinated the acclimation response of many different cells living in a community. The finding of a signaling process, like the ROS wave, in mammalian cells further contributes to our understanding of different diseases and could impact the development of drugs that target for example cancer or heart disease.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Reactive Oxygen Species
*Hydrogen Peroxide
*Signal Transduction
Cell Communication
Plants
Mammals
RevDate: 2023-07-27
The paradox of cooperation among selfish cancer cells.
Evolutionary applications, 16(7):1239-1256.
It is traditionally assumed that during cancer development, tumor cells abort their initially cooperative behavior (i.e., cheat) in favor of evolutionary strategies designed solely to enhance their own fitness (i.e., a "selfish" life style) at the expense of that of the multicellular organism. However, the growth and progress of solid tumors can also involve cooperation among these presumed selfish cells (which, by definition, should be noncooperative) and with stromal cells. The ultimate and proximate reasons behind this paradox are not fully understood. Here, in the light of current theories on the evolution of cooperation, we discuss the possible evolutionary mechanisms that could explain the apparent cooperative behaviors among selfish malignant cells. In addition to the most classical explanations for cooperation in cancer and in general (by-product mutualism, kin selection, direct reciprocity, indirect reciprocity, network reciprocity, group selection), we propose the idea that "greenbeard" effects are relevant to explaining some cooperative behaviors in cancer. Also, we discuss the possibility that malignant cooperative cells express or co-opt cooperative traits normally expressed by healthy cells. We provide examples where considerations of these processes could help understand tumorigenesis and metastasis and argue that this framework provides novel insights into cancer biology and potential strategies for cancer prevention and treatment.
Additional Links: PMID-37492150
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@article {pmid37492150,
year = {2023},
author = {Capp, JP and Thomas, F and Marusyk, A and M Dujon, A and Tissot, S and Gatenby, R and Roche, B and Ujvari, B and DeGregori, J and Brown, JS and Nedelcu, AM},
title = {The paradox of cooperation among selfish cancer cells.},
journal = {Evolutionary applications},
volume = {16},
number = {7},
pages = {1239-1256},
pmid = {37492150},
issn = {1752-4571},
abstract = {It is traditionally assumed that during cancer development, tumor cells abort their initially cooperative behavior (i.e., cheat) in favor of evolutionary strategies designed solely to enhance their own fitness (i.e., a "selfish" life style) at the expense of that of the multicellular organism. However, the growth and progress of solid tumors can also involve cooperation among these presumed selfish cells (which, by definition, should be noncooperative) and with stromal cells. The ultimate and proximate reasons behind this paradox are not fully understood. Here, in the light of current theories on the evolution of cooperation, we discuss the possible evolutionary mechanisms that could explain the apparent cooperative behaviors among selfish malignant cells. In addition to the most classical explanations for cooperation in cancer and in general (by-product mutualism, kin selection, direct reciprocity, indirect reciprocity, network reciprocity, group selection), we propose the idea that "greenbeard" effects are relevant to explaining some cooperative behaviors in cancer. Also, we discuss the possibility that malignant cooperative cells express or co-opt cooperative traits normally expressed by healthy cells. We provide examples where considerations of these processes could help understand tumorigenesis and metastasis and argue that this framework provides novel insights into cancer biology and potential strategies for cancer prevention and treatment.},
}
RevDate: 2023-07-23
On the origin and evolution of the dual oscillator model underlying the photoperiodic clockwork in the suprachiasmatic nucleus.
Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology [Epub ahead of print].
Decades have now passed since Colin Pittendrigh first proposed a model of a circadian clock composed of two coupled oscillators, individually responsive to the rising and setting sun, as a flexible solution to the challenge of behavioral and physiological adaptation to the changing seasons. The elegance and predictive power of this postulation has stimulated laboratories around the world in searches to identify and localize such hypothesized evening and morning oscillators, or sets of oscillators, in insects, rodents, and humans, with experimental designs and approaches keeping pace over the years with technological advances in biology and neuroscience. Here, we recount the conceptual origin and highlight the subsequent evolution of this dual oscillator model for the circadian clock in the mammalian suprachiasmatic nucleus; and how, despite our increasingly sophisticated view of this multicellular pacemaker, Pittendrigh's binary conception has remained influential in our clock models and metaphors.
Additional Links: PMID-37481773
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@article {pmid37481773,
year = {2023},
author = {Evans, JA and Schwartz, WJ},
title = {On the origin and evolution of the dual oscillator model underlying the photoperiodic clockwork in the suprachiasmatic nucleus.},
journal = {Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology},
volume = {},
number = {},
pages = {},
pmid = {37481773},
issn = {1432-1351},
support = {R01GM143545/NH/NIH HHS/United States ; },
abstract = {Decades have now passed since Colin Pittendrigh first proposed a model of a circadian clock composed of two coupled oscillators, individually responsive to the rising and setting sun, as a flexible solution to the challenge of behavioral and physiological adaptation to the changing seasons. The elegance and predictive power of this postulation has stimulated laboratories around the world in searches to identify and localize such hypothesized evening and morning oscillators, or sets of oscillators, in insects, rodents, and humans, with experimental designs and approaches keeping pace over the years with technological advances in biology and neuroscience. Here, we recount the conceptual origin and highlight the subsequent evolution of this dual oscillator model for the circadian clock in the mammalian suprachiasmatic nucleus; and how, despite our increasingly sophisticated view of this multicellular pacemaker, Pittendrigh's binary conception has remained influential in our clock models and metaphors.},
}
RevDate: 2023-07-28
The molecular basis of tumor metastasis and current approaches to decode targeted migration-promoting events in pediatric neuroblastoma.
Biochemical pharmacology, 215:115696 pii:S0006-2952(23)00287-3 [Epub ahead of print].
Cell motility is a crucial biological process that plays a critical role in the development of multicellular organisms and is essential for tissue formation and regeneration. However, uncontrolled cell motility can lead to the development of various diseases, including neoplasms. In this review, we discuss recent advances in the discovery of regulatory mechanisms underlying the metastatic spread of neuroblastoma, a solid pediatric tumor that originates in the embryonic migratory cells of the neural crest. The highly motile phenotype of metastatic neuroblastoma cells requires targeting of intracellular and extracellular processes, that, if affected, would be helpful for the treatment of high-risk patients with neuroblastoma, for whom current therapies remain inadequate. Development of new potentially migration-inhibiting compounds and standardized preclinical approaches for the selection of anti-metastatic drugs in neuroblastoma will also be discussed.
Additional Links: PMID-37481138
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@article {pmid37481138,
year = {2023},
author = {Corallo, D and Dalla Vecchia, M and Lazic, D and Taschner-Mandl, S and Biffi, A and Aveic, S},
title = {The molecular basis of tumor metastasis and current approaches to decode targeted migration-promoting events in pediatric neuroblastoma.},
journal = {Biochemical pharmacology},
volume = {215},
number = {},
pages = {115696},
doi = {10.1016/j.bcp.2023.115696},
pmid = {37481138},
issn = {1873-2968},
abstract = {Cell motility is a crucial biological process that plays a critical role in the development of multicellular organisms and is essential for tissue formation and regeneration. However, uncontrolled cell motility can lead to the development of various diseases, including neoplasms. In this review, we discuss recent advances in the discovery of regulatory mechanisms underlying the metastatic spread of neuroblastoma, a solid pediatric tumor that originates in the embryonic migratory cells of the neural crest. The highly motile phenotype of metastatic neuroblastoma cells requires targeting of intracellular and extracellular processes, that, if affected, would be helpful for the treatment of high-risk patients with neuroblastoma, for whom current therapies remain inadequate. Development of new potentially migration-inhibiting compounds and standardized preclinical approaches for the selection of anti-metastatic drugs in neuroblastoma will also be discussed.},
}
RevDate: 2023-07-21
Regulation of lipid synthesis in myelin modulates neural activity and is required for motor learning.
Glia [Epub ahead of print].
Brain function relies on both rapid electrical communication in neural circuitry and appropriate patterns or synchrony of neural activity. Rapid communication between neurons is facilitated by wrapping nerve axons with insulation by a myelin sheath composed largely of different lipids. Recent evidence has indicated that the extent of myelination of nerve axons can adapt based on neural activity levels and this adaptive myelination is associated with improved learning of motor tasks, suggesting such plasticity may enhance effective learning. In this study, we examined whether another aspect of myelin plasticity-changes in myelin lipid synthesis and composition-may also be associated with motor learning. We combined a motor learning task in mice with in vivo two-photon imaging of neural activity in the primary motor cortex (M1) to distinguish early and late stages of learning and then probed levels of some key myelin lipids using mass spectrometry analysis. Sphingomyelin levels were elevated in the early stage of motor learning while galactosylceramide levels were elevated in the middle and late stages of motor learning, and these changes were correlated across individual mice with both learning performance and neural activity changes. Targeted inhibition of oligodendrocyte-specific galactosyltransferase expression, the enzyme that synthesizes myelin galactosylceramide, impaired motor learning. Our results suggest regulation of myelin lipid composition could be a novel facet of myelin adaptations associated with learning.
Additional Links: PMID-37475643
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@article {pmid37475643,
year = {2023},
author = {Kato, D and Aoyama, Y and Nishida, K and Takahashi, Y and Sakamoto, T and Takeda, I and Tatematsu, T and Go, S and Saito, Y and Kunishima, S and Cheng, J and Hou, L and Tachibana, Y and Sugio, S and Kondo, R and Eto, F and Sato, S and Moorhouse, AJ and Yao, I and Kadomatsu, K and Setou, M and Wake, H},
title = {Regulation of lipid synthesis in myelin modulates neural activity and is required for motor learning.},
journal = {Glia},
volume = {},
number = {},
pages = {},
doi = {10.1002/glia.24441},
pmid = {37475643},
issn = {1098-1136},
support = {JPMJCR1755//Core Research for Evolutional Science and Technology/ ; JPMJCR22P6//Core Research for Evolutional Science and Technology/ ; 20H05699//Grants-in-Aid for Transformative Research Areas (A)/ ; 21H05587//Grants-in-Aid for Transformative Research Areas (A)/ ; JP23gm1410011 h0002//Japan Agency for Medical Research and Development/ ; JP22ak0101150//Japan Agency for Medical Research and Development/ ; 26710004//Grants-in-Aid for Young Scientists (A)/ ; JPMJFR2145//FOREST program/ ; 20K16574//Grants-in-Aid for Young Scientists/ ; //Nagoya University CIBoG WISE program from MEXT/ ; 25110732//Grants-in-Aid for Scientific Research on Innovative Areas/ ; 19H05219//Grants-in-Aid for Scientific Research on Innovative Areas/ ; 19H04753//Grants-in-Aid for Scientific Research on Innovative Areas/ ; 20KK0170//Fostering Joint International Research (B)/ ; 21H02662//Grants-in-Aid for Scientific Research (B)/ ; 18H02598//Grants-in-Aid for Scientific Research (B)/ ; },
abstract = {Brain function relies on both rapid electrical communication in neural circuitry and appropriate patterns or synchrony of neural activity. Rapid communication between neurons is facilitated by wrapping nerve axons with insulation by a myelin sheath composed largely of different lipids. Recent evidence has indicated that the extent of myelination of nerve axons can adapt based on neural activity levels and this adaptive myelination is associated with improved learning of motor tasks, suggesting such plasticity may enhance effective learning. In this study, we examined whether another aspect of myelin plasticity-changes in myelin lipid synthesis and composition-may also be associated with motor learning. We combined a motor learning task in mice with in vivo two-photon imaging of neural activity in the primary motor cortex (M1) to distinguish early and late stages of learning and then probed levels of some key myelin lipids using mass spectrometry analysis. Sphingomyelin levels were elevated in the early stage of motor learning while galactosylceramide levels were elevated in the middle and late stages of motor learning, and these changes were correlated across individual mice with both learning performance and neural activity changes. Targeted inhibition of oligodendrocyte-specific galactosyltransferase expression, the enzyme that synthesizes myelin galactosylceramide, impaired motor learning. Our results suggest regulation of myelin lipid composition could be a novel facet of myelin adaptations associated with learning.},
}
RevDate: 2023-07-26
CmpDate: 2023-07-21
Evolution of selfish multicellularity: collective organisation of individual spatio-temporal regulatory strategies.
BMC ecology and evolution, 23(1):35.
BACKGROUND: The unicellular ancestors of modern-day multicellular organisms were remarkably complex. They had an extensive set of regulatory and signalling genes, an intricate life cycle and could change their behaviour in response to environmental changes. At the transition to multicellularity, some of these behaviours were co-opted to organise the development of the nascent multicellular organism. Here, we focus on the transition to multicellularity before the evolution of stable cell differentiation, to reveal how the emergence of clusters affects the evolution of cell behaviour.
RESULTS: We construct a computational model of a population of cells that can evolve the regulation of their behavioural state - either division or migration - and study both a unicellular and a multicellular context. Cells compete for reproduction and for resources to survive in a seasonally changing environment. We find that the evolution of multicellularity strongly determines the co-evolution of cell behaviour, by altering the competition dynamics between cells. When adhesion cannot evolve, cells compete for survival by rapidly migrating towards resources before dividing. When adhesion evolves, emergent collective migration alleviates the pressure on individual cells to reach resources. This allows individual cells to maximise their own replication. Migrating adhesive clusters display striking patterns of spatio-temporal cell state changes that visually resemble animal development.
CONCLUSIONS: Our model demonstrates how emergent selection pressures at the onset of multicellularity can drive the evolution of cellular behaviour to give rise to developmental patterns.
Additional Links: PMID-37468829
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@article {pmid37468829,
year = {2023},
author = {Vroomans, RMA and Colizzi, ES},
title = {Evolution of selfish multicellularity: collective organisation of individual spatio-temporal regulatory strategies.},
journal = {BMC ecology and evolution},
volume = {23},
number = {1},
pages = {35},
pmid = {37468829},
issn = {2730-7182},
mesh = {Animals ; *Biological Evolution ; *Reproduction ; Cell Differentiation ; },
abstract = {BACKGROUND: The unicellular ancestors of modern-day multicellular organisms were remarkably complex. They had an extensive set of regulatory and signalling genes, an intricate life cycle and could change their behaviour in response to environmental changes. At the transition to multicellularity, some of these behaviours were co-opted to organise the development of the nascent multicellular organism. Here, we focus on the transition to multicellularity before the evolution of stable cell differentiation, to reveal how the emergence of clusters affects the evolution of cell behaviour.
RESULTS: We construct a computational model of a population of cells that can evolve the regulation of their behavioural state - either division or migration - and study both a unicellular and a multicellular context. Cells compete for reproduction and for resources to survive in a seasonally changing environment. We find that the evolution of multicellularity strongly determines the co-evolution of cell behaviour, by altering the competition dynamics between cells. When adhesion cannot evolve, cells compete for survival by rapidly migrating towards resources before dividing. When adhesion evolves, emergent collective migration alleviates the pressure on individual cells to reach resources. This allows individual cells to maximise their own replication. Migrating adhesive clusters display striking patterns of spatio-temporal cell state changes that visually resemble animal development.
CONCLUSIONS: Our model demonstrates how emergent selection pressures at the onset of multicellularity can drive the evolution of cellular behaviour to give rise to developmental patterns.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Biological Evolution
*Reproduction
Cell Differentiation
RevDate: 2023-07-20
Gravity's effect on biology.
Frontiers in physiology, 14:1199175.
Gravity is a fundamental interaction that permeates throughout our Universe. On Earth, gravity gives weight to physical objects, and has been a constant presence throughout terrestrial biological evolution. Thus, gravity has shaped all biological functions, some examples include the growth of plants (e.g., gravitropism), the structure and morphology of biological parts in multicellular organisms, to its effects on our physiological function when humans travel into space. Moreover, from an evolutionary perspective, gravity has been a constant force on biology, and life, to our understanding, should have no reason to not experience the effects of gravity. Interestingly, there appear to be specific biological mechanisms that activate in the absence of gravity, with the space environment the only location to study the effects of a lack of gravity on biological systems. Thus, in this perspective piece, biological adaptations from the cellular to the whole organism levels to the presence and absence of gravity will be organized and described, as well as outlining future areas of research for gravitational biological investigations to address. Up to now, we have observed and shown how gravity effects biology at different levels, with a few examples including genetic (e.g., cell cycle, metabolism, signal transduction associated pathways, etc.), biochemically (e.g., cytoskeleton, NADPH oxidase, Yes-associated protein, etc.), and functionally (e.g., astronauts experiencing musculoskeletal and cardiovascular deconditioning, immune dysfunction, etc., when traveling into space). Based from these observations, there appear to be gravity-sensitive and specific pathways across biological organisms, though knowledge gaps of the effects of gravity on biology remain, such as similarities and differences across species, reproduction, development, and evolutionary adaptations, sex-differences, etc. Thus, here an overview of the literature is provided for context of gravitational biology research to-date and consideration for future studies, as we prepare for long-term occupation of low-Earth Orbit and cis-Lunar space, and missions to the Moon and Mars, experiencing the effects of Lunar and Martian gravity on biology, respectively, through our Artemis program.
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@article {pmid37465696,
year = {2023},
author = {Narayanan, SA},
title = {Gravity's effect on biology.},
journal = {Frontiers in physiology},
volume = {14},
number = {},
pages = {1199175},
pmid = {37465696},
issn = {1664-042X},
abstract = {Gravity is a fundamental interaction that permeates throughout our Universe. On Earth, gravity gives weight to physical objects, and has been a constant presence throughout terrestrial biological evolution. Thus, gravity has shaped all biological functions, some examples include the growth of plants (e.g., gravitropism), the structure and morphology of biological parts in multicellular organisms, to its effects on our physiological function when humans travel into space. Moreover, from an evolutionary perspective, gravity has been a constant force on biology, and life, to our understanding, should have no reason to not experience the effects of gravity. Interestingly, there appear to be specific biological mechanisms that activate in the absence of gravity, with the space environment the only location to study the effects of a lack of gravity on biological systems. Thus, in this perspective piece, biological adaptations from the cellular to the whole organism levels to the presence and absence of gravity will be organized and described, as well as outlining future areas of research for gravitational biological investigations to address. Up to now, we have observed and shown how gravity effects biology at different levels, with a few examples including genetic (e.g., cell cycle, metabolism, signal transduction associated pathways, etc.), biochemically (e.g., cytoskeleton, NADPH oxidase, Yes-associated protein, etc.), and functionally (e.g., astronauts experiencing musculoskeletal and cardiovascular deconditioning, immune dysfunction, etc., when traveling into space). Based from these observations, there appear to be gravity-sensitive and specific pathways across biological organisms, though knowledge gaps of the effects of gravity on biology remain, such as similarities and differences across species, reproduction, development, and evolutionary adaptations, sex-differences, etc. Thus, here an overview of the literature is provided for context of gravitational biology research to-date and consideration for future studies, as we prepare for long-term occupation of low-Earth Orbit and cis-Lunar space, and missions to the Moon and Mars, experiencing the effects of Lunar and Martian gravity on biology, respectively, through our Artemis program.},
}
RevDate: 2023-07-27
Cancer Prevalence Across Vertebrates.
Research square.
Cancer is pervasive across multicellular species, but what explains differences in cancer prevalence across species? Using 16,049 necropsy records for 292 species spanning three clades (amphibians, sauropsids and mammals) we found that neoplasia and malignancy prevalence increases with adult weight (contrary to Peto's Paradox) and somatic mutation rate, but decreases with gestation time. Evolution of cancer susceptibility appears to have undergone sudden shifts followed by stabilizing selection. Outliers for neoplasia prevalence include the common porpoise (<1.3%), the Rodrigues fruit bat (<1.6%) the black-footed penguin (<0.4%), ferrets (63%) and opossums (35%). Discovering why some species have particularly high or low levels of cancer may lead to a better understanding of cancer syndromes and novel strategies for the management and prevention of cancer.
Additional Links: PMID-37461608
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@article {pmid37461608,
year = {2023},
author = {Compton, Z and Harris, V and Mellon, W and Rupp, S and Mallo, D and Kapsetaki, S and Wilmot, M and Kennington, R and Noble, K and Baciu, C and Ramirez, L and Peraza, A and Martins, B and Sudhakar, S and Aksoy, S and Furukawa, G and Vincze, O and Giraudeau, M and Duke, E and Spiro, S and Flach, E and Davidson, H and Zehnder, A and Graham, T and Troan, B and Harrison, T and Tollis, M and Schiffman, J and Aktipis, A and Abegglen, L and Maley, C and Boddy, A},
title = {Cancer Prevalence Across Vertebrates.},
journal = {Research square},
volume = {},
number = {},
pages = {},
pmid = {37461608},
abstract = {Cancer is pervasive across multicellular species, but what explains differences in cancer prevalence across species? Using 16,049 necropsy records for 292 species spanning three clades (amphibians, sauropsids and mammals) we found that neoplasia and malignancy prevalence increases with adult weight (contrary to Peto's Paradox) and somatic mutation rate, but decreases with gestation time. Evolution of cancer susceptibility appears to have undergone sudden shifts followed by stabilizing selection. Outliers for neoplasia prevalence include the common porpoise (<1.3%), the Rodrigues fruit bat (<1.6%) the black-footed penguin (<0.4%), ferrets (63%) and opossums (35%). Discovering why some species have particularly high or low levels of cancer may lead to a better understanding of cancer syndromes and novel strategies for the management and prevention of cancer.},
}
RevDate: 2023-07-29
CmpDate: 2023-07-19
Geometrical control of interface patterning underlies active matter invasion.
Proceedings of the National Academy of Sciences of the United States of America, 120(30):e2219708120.
Interaction between active materials and the boundaries of geometrical confinement is key to many emergent phenomena in active systems. For living active matter consisting of animal cells or motile bacteria, the confinement boundary is often a deformable interface, and it has been unclear how activity-induced interface dynamics might lead to morphogenesis and pattern formation. Here, we studied the evolution of bacterial active matter confined by a deformable boundary. We found that an ordered morphological pattern emerged at the interface characterized by periodically spaced interfacial protrusions; behind the interfacial protrusions, bacterial swimmers self-organized into multicellular clusters displaying +1/2 nematic defects. Subsequently, a hierarchical sequence of transitions from interfacial protrusions to creeping branches allowed the bacterial active drop to rapidly invade surrounding space with a striking self-similar branch pattern. We found that this interface patterning is geometrically controlled by the local curvature of the interface, a phenomenon we denote as collective curvature sensing. Using a continuum active model, we revealed that the collective curvature sensing arises from enhanced active stresses near high-curvature regions, with the active length scale setting the characteristic distance between the interfacial protrusions. Our findings reveal a protrusion-to-branch transition as a unique mode of active matter invasion and suggest a strategy to engineer pattern formation of active materials.
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@article {pmid37459530,
year = {2023},
author = {Xu, H and Nejad, MR and Yeomans, JM and Wu, Y},
title = {Geometrical control of interface patterning underlies active matter invasion.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {120},
number = {30},
pages = {e2219708120},
pmid = {37459530},
issn = {1091-6490},
mesh = {*Bacteria ; },
abstract = {Interaction between active materials and the boundaries of geometrical confinement is key to many emergent phenomena in active systems. For living active matter consisting of animal cells or motile bacteria, the confinement boundary is often a deformable interface, and it has been unclear how activity-induced interface dynamics might lead to morphogenesis and pattern formation. Here, we studied the evolution of bacterial active matter confined by a deformable boundary. We found that an ordered morphological pattern emerged at the interface characterized by periodically spaced interfacial protrusions; behind the interfacial protrusions, bacterial swimmers self-organized into multicellular clusters displaying +1/2 nematic defects. Subsequently, a hierarchical sequence of transitions from interfacial protrusions to creeping branches allowed the bacterial active drop to rapidly invade surrounding space with a striking self-similar branch pattern. We found that this interface patterning is geometrically controlled by the local curvature of the interface, a phenomenon we denote as collective curvature sensing. Using a continuum active model, we revealed that the collective curvature sensing arises from enhanced active stresses near high-curvature regions, with the active length scale setting the characteristic distance between the interfacial protrusions. Our findings reveal a protrusion-to-branch transition as a unique mode of active matter invasion and suggest a strategy to engineer pattern formation of active materials.},
}
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*Bacteria
RevDate: 2023-07-18
CmpDate: 2023-07-17
Talk to Me-Interplay between Mitochondria and Microbiota in Aging.
International journal of molecular sciences, 24(13):.
The existence of mitochondria in eukaryotic host cells as a remnant of former microbial organisms has been widely accepted, as has their fundamental role in several diseases and physiological aging. In recent years, it has become clear that the health, aging, and life span of multicellular hosts are also highly dependent on the still-residing microbiota, e.g., those within the intestinal system. Due to the common evolutionary origin of mitochondria and these microbial commensals, it is intriguing to investigate if there might be a crosstalk based on preserved common properties. In the light of rising knowledge on the gut-brain axis, such crosstalk might severely affect brain homeostasis in aging, as neuronal tissue has a high energy demand and low tolerance for according functional decline. In this review, we summarize what is known about the impact of both mitochondria and the microbiome on the host's aging process and what is known about the aging of both entities. For a long time, bacteria were assumed to be immortal; however, recent evidence indicates their aging and similar observations have been made for mitochondria. Finally, we present pathways by which mitochondria are affected by microbiota and give information about therapeutic anti-aging approaches that are based on current knowledge.
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@article {pmid37445995,
year = {2023},
author = {Endres, K and Friedland, K},
title = {Talk to Me-Interplay between Mitochondria and Microbiota in Aging.},
journal = {International journal of molecular sciences},
volume = {24},
number = {13},
pages = {},
pmid = {37445995},
issn = {1422-0067},
mesh = {*Gastrointestinal Microbiome/physiology ; *Microbiota ; Mitochondria ; Bacteria/metabolism ; },
abstract = {The existence of mitochondria in eukaryotic host cells as a remnant of former microbial organisms has been widely accepted, as has their fundamental role in several diseases and physiological aging. In recent years, it has become clear that the health, aging, and life span of multicellular hosts are also highly dependent on the still-residing microbiota, e.g., those within the intestinal system. Due to the common evolutionary origin of mitochondria and these microbial commensals, it is intriguing to investigate if there might be a crosstalk based on preserved common properties. In the light of rising knowledge on the gut-brain axis, such crosstalk might severely affect brain homeostasis in aging, as neuronal tissue has a high energy demand and low tolerance for according functional decline. In this review, we summarize what is known about the impact of both mitochondria and the microbiome on the host's aging process and what is known about the aging of both entities. For a long time, bacteria were assumed to be immortal; however, recent evidence indicates their aging and similar observations have been made for mitochondria. Finally, we present pathways by which mitochondria are affected by microbiota and give information about therapeutic anti-aging approaches that are based on current knowledge.},
}
MeSH Terms:
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*Gastrointestinal Microbiome/physiology
*Microbiota
Mitochondria
Bacteria/metabolism
RevDate: 2023-07-13
The sporophyte-to-gametophyte transition: The haploid generation comes of age.
Current opinion in plant biology, 75:102416 pii:S1369-5266(23)00081-X [Epub ahead of print].
Flowering plants alternate between two multicellular generations: the diploid sporophyte and haploid gametophyte. Despite its small size, the gametophyte has significant impacts on plant genetics, evolution, and breeding. Each male pollen grain and female embryo sac is a multicellular organism with independent gene expression, a functioning metabolism, and specialized cell types. In this review, we describe recent progress in understanding the process in which the haploid genome takes over expression from its diploid parent - the sporophyte-to-gametophyte transition. The focus is on pollen, but similar concepts may also apply to the female gametophyte. Technological advances in single-cell genomics offer the opportunity to characterize haploid gene expression in unprecedented detail, positioning the field to make rapid progress.
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@article {pmid37441836,
year = {2023},
author = {Somers, J and Nelms, B},
title = {The sporophyte-to-gametophyte transition: The haploid generation comes of age.},
journal = {Current opinion in plant biology},
volume = {75},
number = {},
pages = {102416},
doi = {10.1016/j.pbi.2023.102416},
pmid = {37441836},
issn = {1879-0356},
abstract = {Flowering plants alternate between two multicellular generations: the diploid sporophyte and haploid gametophyte. Despite its small size, the gametophyte has significant impacts on plant genetics, evolution, and breeding. Each male pollen grain and female embryo sac is a multicellular organism with independent gene expression, a functioning metabolism, and specialized cell types. In this review, we describe recent progress in understanding the process in which the haploid genome takes over expression from its diploid parent - the sporophyte-to-gametophyte transition. The focus is on pollen, but similar concepts may also apply to the female gametophyte. Technological advances in single-cell genomics offer the opportunity to characterize haploid gene expression in unprecedented detail, positioning the field to make rapid progress.},
}
RevDate: 2023-07-12
Generating Functional Multicellular Organoids from Human Placenta Villi.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
The interaction between trophoblasts, stroma cells, and immune cells at the maternal-fetal interface constitutes the functional units of the placenta, which is crucial for successful pregnancy outcomes. However, the investigation of this intricate interplay is restricted due to the absence of efficient experimental models. To address this challenge, a robust, reliable methodology for generating placenta villi organoids (PVOs) from early, late, or diseased pregnancies using air-liquid surface culture is developed. PVOs contain cytotrophoblasts that can self-renew and differentiate directly, along with stromal elements that retain native immune cells. Analysis of scRNA sequencing and WES data reveals that PVOs faithfully recapitulate the cellular components and genetic alterations of the corresponding source tissue. Additionally, PVOs derived from patients with preeclampsia exhibit specific pathological features such as inflammation, antiangiogenic imbalance, and decreased syncytin expression. The PVO-based propagation of primary placenta villi should enable a deeper investigation of placenta development and exploration of the underlying pathogenesis and therapeutics of placenta-originated diseases.
Additional Links: PMID-37438660
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@article {pmid37438660,
year = {2023},
author = {Huang, L and Tu, Z and Wei, L and Sun, W and Wang, Y and Bi, S and He, F and Du, L and Chen, J and Kzhyshkowska, J and Wang, H and Chen, D and Zhang, S},
title = {Generating Functional Multicellular Organoids from Human Placenta Villi.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2301565},
doi = {10.1002/advs.202301565},
pmid = {37438660},
issn = {2198-3844},
support = {2022YFC2702501//National Key Research and Development Program of China/ ; 2022YFC2704500//National Key Research and Development Program of China/ ; 81830045//Key Program of National Natural Science Foundation of China/ ; 81071652//National Natural Science Foundation of China/ ; 82171666//National Natural Science Foundation of China/ ; 82201861//National Natural Science Foundation of China/ ; 82271695//National Natural Science Foundation of China/ ; M-0586//Mobility program of Sino German Center/ ; 202201020573//Science and Technology Program of Guangzhou/ ; 2023A03J0378//Science and Technology Program of Guangzhou/ ; 2021B1515120070//China Guangdong Basic and Applied Basic Research Fund/ ; },
abstract = {The interaction between trophoblasts, stroma cells, and immune cells at the maternal-fetal interface constitutes the functional units of the placenta, which is crucial for successful pregnancy outcomes. However, the investigation of this intricate interplay is restricted due to the absence of efficient experimental models. To address this challenge, a robust, reliable methodology for generating placenta villi organoids (PVOs) from early, late, or diseased pregnancies using air-liquid surface culture is developed. PVOs contain cytotrophoblasts that can self-renew and differentiate directly, along with stromal elements that retain native immune cells. Analysis of scRNA sequencing and WES data reveals that PVOs faithfully recapitulate the cellular components and genetic alterations of the corresponding source tissue. Additionally, PVOs derived from patients with preeclampsia exhibit specific pathological features such as inflammation, antiangiogenic imbalance, and decreased syncytin expression. The PVO-based propagation of primary placenta villi should enable a deeper investigation of placenta development and exploration of the underlying pathogenesis and therapeutics of placenta-originated diseases.},
}
RevDate: 2023-07-18
CmpDate: 2023-07-14
A conserved RWP-RK transcription factor VSR1 controls gametic differentiation in volvocine algae.
Proceedings of the National Academy of Sciences of the United States of America, 120(29):e2305099120.
Volvocine green algae are a model for understanding the evolution of mating types and sexes. They are facultatively sexual, with gametic differentiation occurring in response to nitrogen starvation (-N) in most genera and to sex inducer hormone in Volvox. The conserved RWP-RK family transcription factor (TF) MID is encoded by the minus mating-type locus or male sex-determining region of heterothallic volvocine species and dominantly determines minus or male gametic differentiation. However, the factor(s) responsible for establishing the default plus or female differentiation programs have remained elusive. We performed a phylo-transcriptomic screen for autosomal RWP-RK TFs induced during gametogenesis in unicellular isogamous Chlamydomonas reinhardtii (Chlamydomonas) and in multicellular oogamous Volvox carteri (Volvox) and identified a single conserved ortho-group we named Volvocine Sex Regulator 1 (VSR1). Chlamydomonas vsr1 mutants of either mating type failed to mate and could not induce expression of key mating-type-specific genes. Similarly, Volvox vsr1 mutants in either sex could initiate sexual embryogenesis, but the presumptive eggs or androgonidia (sperm packet precursors) were infertile and unable to express key sex-specific genes. Yeast two-hybrid assays identified a conserved domain in VSR1 capable of self-interaction or interaction with the conserved N terminal domain of MID. In vivo coimmunoprecipitation experiments demonstrated association of VSR1 and MID in both Chlamydomonas and Volvox. These data support a new model for volvocine sexual differentiation where VSR1 homodimers activate expression of plus/female gamete-specific-genes, but when MID is present, MID-VSR1 heterodimers are preferentially formed and activate minus/male gamete-specific-genes.
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@article {pmid37436957,
year = {2023},
author = {Geng, S and Hamaji, T and Ferris, PJ and Gao, M and Nishimura, Y and Umen, J},
title = {A conserved RWP-RK transcription factor VSR1 controls gametic differentiation in volvocine algae.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {120},
number = {29},
pages = {e2305099120},
doi = {10.1073/pnas.2305099120},
pmid = {37436957},
issn = {1091-6490},
support = {R01GM078376/NH/NIH HHS/United States ; },
mesh = {*Seeds ; Sex ; Reproduction ; Germ Cells ; Spermatozoa ; Biotin ; *Chlamydomonas ; },
abstract = {Volvocine green algae are a model for understanding the evolution of mating types and sexes. They are facultatively sexual, with gametic differentiation occurring in response to nitrogen starvation (-N) in most genera and to sex inducer hormone in Volvox. The conserved RWP-RK family transcription factor (TF) MID is encoded by the minus mating-type locus or male sex-determining region of heterothallic volvocine species and dominantly determines minus or male gametic differentiation. However, the factor(s) responsible for establishing the default plus or female differentiation programs have remained elusive. We performed a phylo-transcriptomic screen for autosomal RWP-RK TFs induced during gametogenesis in unicellular isogamous Chlamydomonas reinhardtii (Chlamydomonas) and in multicellular oogamous Volvox carteri (Volvox) and identified a single conserved ortho-group we named Volvocine Sex Regulator 1 (VSR1). Chlamydomonas vsr1 mutants of either mating type failed to mate and could not induce expression of key mating-type-specific genes. Similarly, Volvox vsr1 mutants in either sex could initiate sexual embryogenesis, but the presumptive eggs or androgonidia (sperm packet precursors) were infertile and unable to express key sex-specific genes. Yeast two-hybrid assays identified a conserved domain in VSR1 capable of self-interaction or interaction with the conserved N terminal domain of MID. In vivo coimmunoprecipitation experiments demonstrated association of VSR1 and MID in both Chlamydomonas and Volvox. These data support a new model for volvocine sexual differentiation where VSR1 homodimers activate expression of plus/female gamete-specific-genes, but when MID is present, MID-VSR1 heterodimers are preferentially formed and activate minus/male gamete-specific-genes.},
}
MeSH Terms:
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*Seeds
Sex
Reproduction
Germ Cells
Spermatozoa
Biotin
*Chlamydomonas
RevDate: 2023-07-13
Generalizing the Domain-Gene-Species Reconciliation Framework to Microbial Genes and Domains.
IEEE/ACM transactions on computational biology and bioinformatics, PP: [Epub ahead of print].
Protein domains play an important role in the function and evolution of many gene families. Previous studies have shown that domains are frequently lost or gained during gene family evolution. Yet, most computational approaches for studying gene family evolution do not account for domain-level evolution within genes. To address this limitation, a new three-level reconciliation framework, called the Domain-Gene-Species (DGS) reconciliation model, has been recently developed to simultaneously model the evolution of a domain family inside one or more gene families and the evolution of those gene families inside a species tree. However, the existing model applies only to multi-cellular eukaryotes where horizontal gene transfer is negligible. In this work, we generalize the existing DGS reconciliation model by allowing for the spread of genes and domains across species boundaries through horizontal transfer. We show that the problem of computing optimal generalized DGS reconciliations, though NP-hard, is approximable to within a constant factor, where the specific approximation ratio depends on the "event costs" used. We provide two different approximation algorithms for the problem and demonstrate the impact of the generalized framework using both simulated and real biological data. Our results show that our new algorithms result in highly accurate reconstructions of domain family evolution for microbes.
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@article {pmid37436868,
year = {2023},
author = {Mondal, A and Bansal, MS},
title = {Generalizing the Domain-Gene-Species Reconciliation Framework to Microbial Genes and Domains.},
journal = {IEEE/ACM transactions on computational biology and bioinformatics},
volume = {PP},
number = {},
pages = {},
doi = {10.1109/TCBB.2023.3294480},
pmid = {37436868},
issn = {1557-9964},
abstract = {Protein domains play an important role in the function and evolution of many gene families. Previous studies have shown that domains are frequently lost or gained during gene family evolution. Yet, most computational approaches for studying gene family evolution do not account for domain-level evolution within genes. To address this limitation, a new three-level reconciliation framework, called the Domain-Gene-Species (DGS) reconciliation model, has been recently developed to simultaneously model the evolution of a domain family inside one or more gene families and the evolution of those gene families inside a species tree. However, the existing model applies only to multi-cellular eukaryotes where horizontal gene transfer is negligible. In this work, we generalize the existing DGS reconciliation model by allowing for the spread of genes and domains across species boundaries through horizontal transfer. We show that the problem of computing optimal generalized DGS reconciliations, though NP-hard, is approximable to within a constant factor, where the specific approximation ratio depends on the "event costs" used. We provide two different approximation algorithms for the problem and demonstrate the impact of the generalized framework using both simulated and real biological data. Our results show that our new algorithms result in highly accurate reconstructions of domain family evolution for microbes.},
}
RevDate: 2023-07-18
Coordinated linear and rotational movements of endothelial cells compartmentalized by VE-cadherin drive angiogenic sprouting.
iScience, 26(7):107051.
Angiogenesis is a sequential process to extend new blood vessels from preexisting ones by sprouting and branching. During angiogenesis, endothelial cells (ECs) exhibit inhomogeneous multicellular behaviors referred to as "cell mixing," in which ECs repetitively exchange their relative positions, but the underlying mechanism remains elusive. Here we identified the coordinated linear and rotational movements potentiated by cell-cell contact as drivers of sprouting angiogenesis using in vitro and in silico approaches. VE-cadherin confers the coordinated linear motility that facilitated forward sprout elongation, although it is dispensable for rotational movement, which was synchronous without VE-cadherin. Mathematical modeling recapitulated the EC motility in the two-cell state and angiogenic morphogenesis with the effects of VE-cadherin-knockout. Finally, we found that VE-cadherin-dependent EC compartmentalization potentiated branch elongations, and confirmed this by mathematical simulation. Collectively, we propose a way to understand angiogenesis, based on unique EC behavioral properties that are partially dependent on VE-cadherin function.
Additional Links: PMID-37426350
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@article {pmid37426350,
year = {2023},
author = {Tonami, K and Hayashi, T and Uchijima, Y and Kanai, M and Yura, F and Mada, J and Sugahara, K and Kurihara, Y and Kominami, Y and Ushijima, T and Takubo, N and Liu, X and Tozawa, H and Kanai, Y and Tokihiro, T and Kurihara, H},
title = {Coordinated linear and rotational movements of endothelial cells compartmentalized by VE-cadherin drive angiogenic sprouting.},
journal = {iScience},
volume = {26},
number = {7},
pages = {107051},
pmid = {37426350},
issn = {2589-0042},
abstract = {Angiogenesis is a sequential process to extend new blood vessels from preexisting ones by sprouting and branching. During angiogenesis, endothelial cells (ECs) exhibit inhomogeneous multicellular behaviors referred to as "cell mixing," in which ECs repetitively exchange their relative positions, but the underlying mechanism remains elusive. Here we identified the coordinated linear and rotational movements potentiated by cell-cell contact as drivers of sprouting angiogenesis using in vitro and in silico approaches. VE-cadherin confers the coordinated linear motility that facilitated forward sprout elongation, although it is dispensable for rotational movement, which was synchronous without VE-cadherin. Mathematical modeling recapitulated the EC motility in the two-cell state and angiogenic morphogenesis with the effects of VE-cadherin-knockout. Finally, we found that VE-cadherin-dependent EC compartmentalization potentiated branch elongations, and confirmed this by mathematical simulation. Collectively, we propose a way to understand angiogenesis, based on unique EC behavioral properties that are partially dependent on VE-cadherin function.},
}
RevDate: 2023-07-06
Longevity of Fungal Mycelia and Nuclear Quality Checks: a New Hypothesis for the Role of Clamp Connections in Dikaryons.
Microbiology and molecular biology reviews : MMBR [Epub ahead of print].
This paper addresses the stability of mycelial growth in fungi and differences between ascomycetes and basidiomycetes. Starting with general evolutionary theories of multicellularity and the role of sex, we then discuss individuality in fungi. Recent research has demonstrated the deleterious consequences of nucleus-level selection in fungal mycelia, favoring cheaters with a nucleus-level benefit during spore formation but a negative effect on mycelium-level fitness. Cheaters appear to generally be loss-of-fusion (LOF) mutants, with a higher propensity to form aerial hyphae developing into asexual spores. Since LOF mutants rely on heterokaryosis with wild-type nuclei, we argue that regular single-spore bottlenecks can efficiently select against such cheater mutants. We then zoom in on ecological differences between ascomycetes being typically fast-growing but short-lived with frequent asexual-spore bottlenecks and basidiomycetes being generally slow-growing but long-lived and usually without asexual-spore bottlenecks. We argue that these life history differences have coevolved with stricter nuclear quality checks in basidiomycetes. Specifically, we propose a new function for clamp connections, structures formed during the sexual stage in ascomycetes and basidiomycetes but during somatic growth only in basidiomycete dikaryons. During dikaryon cell division, the two haploid nuclei temporarily enter a monokaryotic phase, by alternatingly entering a retrograde-growing clamp cell, which subsequently fuses with the subapical cell to recover the dikaryotic cell. We hypothesize that clamp connections act as screening devices for nuclear quality, with both nuclei continuously testing each other for fusion ability, a test that LOF mutants will fail. By linking differences in longevity of the mycelial phase to ecology and stringency of nuclear quality checks, we propose that mycelia have a constant and low lifetime cheating risk, irrespective of their size and longevity.
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@article {pmid37409939,
year = {2023},
author = {Aanen, DK and van 't Padje, A and Auxier, B},
title = {Longevity of Fungal Mycelia and Nuclear Quality Checks: a New Hypothesis for the Role of Clamp Connections in Dikaryons.},
journal = {Microbiology and molecular biology reviews : MMBR},
volume = {},
number = {},
pages = {e0002221},
doi = {10.1128/mmbr.00022-21},
pmid = {37409939},
issn = {1098-5557},
abstract = {This paper addresses the stability of mycelial growth in fungi and differences between ascomycetes and basidiomycetes. Starting with general evolutionary theories of multicellularity and the role of sex, we then discuss individuality in fungi. Recent research has demonstrated the deleterious consequences of nucleus-level selection in fungal mycelia, favoring cheaters with a nucleus-level benefit during spore formation but a negative effect on mycelium-level fitness. Cheaters appear to generally be loss-of-fusion (LOF) mutants, with a higher propensity to form aerial hyphae developing into asexual spores. Since LOF mutants rely on heterokaryosis with wild-type nuclei, we argue that regular single-spore bottlenecks can efficiently select against such cheater mutants. We then zoom in on ecological differences between ascomycetes being typically fast-growing but short-lived with frequent asexual-spore bottlenecks and basidiomycetes being generally slow-growing but long-lived and usually without asexual-spore bottlenecks. We argue that these life history differences have coevolved with stricter nuclear quality checks in basidiomycetes. Specifically, we propose a new function for clamp connections, structures formed during the sexual stage in ascomycetes and basidiomycetes but during somatic growth only in basidiomycete dikaryons. During dikaryon cell division, the two haploid nuclei temporarily enter a monokaryotic phase, by alternatingly entering a retrograde-growing clamp cell, which subsequently fuses with the subapical cell to recover the dikaryotic cell. We hypothesize that clamp connections act as screening devices for nuclear quality, with both nuclei continuously testing each other for fusion ability, a test that LOF mutants will fail. By linking differences in longevity of the mycelial phase to ecology and stringency of nuclear quality checks, we propose that mycelia have a constant and low lifetime cheating risk, irrespective of their size and longevity.},
}
RevDate: 2023-07-05
The Origin of Metazoan Multicellularity: A Potential Microbial Black Swan Event.
Annual review of microbiology [Epub ahead of print].
The emergence of animals from their unicellular ancestors is a major evolutionary event. Thanks to the study of diverse close unicellular relatives of animals, we now have a better grasp of what the unicellular ancestor of animals was like. However, it is unclear how that unicellular ancestor of animals became the first animals. To explain this transition, two popular theories, the choanoblastaea and the synzoospore, have been proposed. We will revise and expose the flaws in these two theories while showing that, due to the limits of our current knowledge, the origin of animals is a biological black swan event. As such, the origin of animals defies retrospective explanations. Therefore, we should be extra careful not to fall for confirmation biases based on few data and, instead, embrace this uncertainty and be open to alternative scenarios. With the aim to broaden the potential explanations on how animals emerged, we here propose two novel and alternative scenarios. In any case, to find the answer to how animals evolved, additional data will be required, as will the hunt for microscopic creatures that are closely related to animals but have not yet been sampled and studied. Expected final online publication date for the Annual Review of Microbiology, Volume 77 is September 2023. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
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@article {pmid37406343,
year = {2023},
author = {Ruiz-Trillo, I and Kin, K and Casacuberta, E},
title = {The Origin of Metazoan Multicellularity: A Potential Microbial Black Swan Event.},
journal = {Annual review of microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1146/annurev-micro-032421-120023},
pmid = {37406343},
issn = {1545-3251},
abstract = {The emergence of animals from their unicellular ancestors is a major evolutionary event. Thanks to the study of diverse close unicellular relatives of animals, we now have a better grasp of what the unicellular ancestor of animals was like. However, it is unclear how that unicellular ancestor of animals became the first animals. To explain this transition, two popular theories, the choanoblastaea and the synzoospore, have been proposed. We will revise and expose the flaws in these two theories while showing that, due to the limits of our current knowledge, the origin of animals is a biological black swan event. As such, the origin of animals defies retrospective explanations. Therefore, we should be extra careful not to fall for confirmation biases based on few data and, instead, embrace this uncertainty and be open to alternative scenarios. With the aim to broaden the potential explanations on how animals emerged, we here propose two novel and alternative scenarios. In any case, to find the answer to how animals evolved, additional data will be required, as will the hunt for microscopic creatures that are closely related to animals but have not yet been sampled and studied. Expected final online publication date for the Annual Review of Microbiology, Volume 77 is September 2023. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.},
}
RevDate: 2023-07-18
Identification and characterization of enhancer elements controlling cell type-specific and signalling dependent chromatin programming during hematopoietic development.
Stem cell investigation, 10:14.
The development of multi-cellular organisms from a single fertilized egg requires to differentially execute the information encoded in our DNA. This complex process is regulated by the interplay of transcription factors with a chromatin environment, both of which provide the epigenetic information maintaining cell-type specific gene expression patterns. Moreover, transcription factors and their target genes form vast interacting gene regulatory networks which can be exquisitely stable. However, all developmental processes originate from pluripotent precursor cell types. The production of terminally differentiated cells from such cells, therefore, requires successive changes of cell fates, meaning that genes relevant for the next stage of differentiation must be switched on and genes not relevant anymore must be switched off. The stimulus for the change of cell fate originates from extrinsic signals which set a cascade of intracellular processes in motion that eventually terminate at the genome leading to changes in gene expression and the development of alternate gene regulatory networks. How developmental trajectories are encoded in the genome and how the interplay between intrinsic and extrinsic processes regulates development is one of the major questions in developmental biology. The development of the hematopoietic system has long served as model to understand how changes in gene regulatory networks drive the differentiation of the various blood cell types. In this review, we highlight the main signals and transcription factors and how they are integrated at the level of chromatin programming and gene expression control. We also highlight recent studies identifying the cis-regulatory elements such as enhancers at the global level and explain how their developmental activity is regulated by the cooperation of cell-type specific and ubiquitous transcription factors with extrinsic signals.
Additional Links: PMID-37404470
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@article {pmid37404470,
year = {2023},
author = {Maytum, A and Edginton-White, B and Bonifer, C},
title = {Identification and characterization of enhancer elements controlling cell type-specific and signalling dependent chromatin programming during hematopoietic development.},
journal = {Stem cell investigation},
volume = {10},
number = {},
pages = {14},
pmid = {37404470},
issn = {2306-9759},
abstract = {The development of multi-cellular organisms from a single fertilized egg requires to differentially execute the information encoded in our DNA. This complex process is regulated by the interplay of transcription factors with a chromatin environment, both of which provide the epigenetic information maintaining cell-type specific gene expression patterns. Moreover, transcription factors and their target genes form vast interacting gene regulatory networks which can be exquisitely stable. However, all developmental processes originate from pluripotent precursor cell types. The production of terminally differentiated cells from such cells, therefore, requires successive changes of cell fates, meaning that genes relevant for the next stage of differentiation must be switched on and genes not relevant anymore must be switched off. The stimulus for the change of cell fate originates from extrinsic signals which set a cascade of intracellular processes in motion that eventually terminate at the genome leading to changes in gene expression and the development of alternate gene regulatory networks. How developmental trajectories are encoded in the genome and how the interplay between intrinsic and extrinsic processes regulates development is one of the major questions in developmental biology. The development of the hematopoietic system has long served as model to understand how changes in gene regulatory networks drive the differentiation of the various blood cell types. In this review, we highlight the main signals and transcription factors and how they are integrated at the level of chromatin programming and gene expression control. We also highlight recent studies identifying the cis-regulatory elements such as enhancers at the global level and explain how their developmental activity is regulated by the cooperation of cell-type specific and ubiquitous transcription factors with extrinsic signals.},
}
RevDate: 2023-07-18
CmpDate: 2023-07-06
High-throughput library transgenesis in Caenorhabditis elegans via Transgenic Arrays Resulting in Diversity of Integrated Sequences (TARDIS).
eLife, 12:.
High-throughput transgenesis using synthetic DNA libraries is a powerful method for systematically exploring genetic function. Diverse synthesized libraries have been used for protein engineering, identification of protein-protein interactions, characterization of promoter libraries, developmental and evolutionary lineage tracking, and various other exploratory assays. However, the need for library transgenesis has effectively restricted these approaches to single-cell models. Here, we present Transgenic Arrays Resulting in Diversity of Integrated Sequences (TARDIS), a simple yet powerful approach to large-scale transgenesis that overcomes typical limitations encountered in multicellular systems. TARDIS splits the transgenesis process into a two-step process: creation of individuals carrying experimentally introduced sequence libraries, followed by inducible extraction and integration of individual sequences/library components from the larger library cassette into engineered genomic sites. Thus, transformation of a single individual, followed by lineage expansion and functional transgenesis, gives rise to thousands of genetically unique transgenic individuals. We demonstrate the power of this system using engineered, split selectable TARDIS sites in Caenorhabditis elegans to generate (1) a large set of individually barcoded lineages and (2) transcriptional reporter lines from predefined promoter libraries. We find that this approach increases transformation yields up to approximately 1000-fold over current single-step methods. While we demonstrate the utility of TARDIS using C. elegans, in principle the process is adaptable to any system where experimentally generated genomic loci landing pads and diverse, heritable DNA elements can be generated.
Additional Links: PMID-37401921
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Citation:
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@article {pmid37401921,
year = {2023},
author = {Stevenson, ZC and Moerdyk-Schauwecker, MJ and Banse, SA and Patel, DS and Lu, H and Phillips, PC},
title = {High-throughput library transgenesis in Caenorhabditis elegans via Transgenic Arrays Resulting in Diversity of Integrated Sequences (TARDIS).},
journal = {eLife},
volume = {12},
number = {},
pages = {},
pmid = {37401921},
issn = {2050-084X},
support = {R01 AG056436/AG/NIA NIH HHS/United States ; R35 GM131838/GM/NIGMS NIH HHS/United States ; R01AG056436/NH/NIH HHS/United States ; R35GM131838/NH/NIH HHS/United States ; },
mesh = {Humans ; Animals ; *Caenorhabditis elegans/genetics ; Transgenes ; Animals, Genetically Modified ; *Gene Transfer Techniques ; Gene Library ; },
abstract = {High-throughput transgenesis using synthetic DNA libraries is a powerful method for systematically exploring genetic function. Diverse synthesized libraries have been used for protein engineering, identification of protein-protein interactions, characterization of promoter libraries, developmental and evolutionary lineage tracking, and various other exploratory assays. However, the need for library transgenesis has effectively restricted these approaches to single-cell models. Here, we present Transgenic Arrays Resulting in Diversity of Integrated Sequences (TARDIS), a simple yet powerful approach to large-scale transgenesis that overcomes typical limitations encountered in multicellular systems. TARDIS splits the transgenesis process into a two-step process: creation of individuals carrying experimentally introduced sequence libraries, followed by inducible extraction and integration of individual sequences/library components from the larger library cassette into engineered genomic sites. Thus, transformation of a single individual, followed by lineage expansion and functional transgenesis, gives rise to thousands of genetically unique transgenic individuals. We demonstrate the power of this system using engineered, split selectable TARDIS sites in Caenorhabditis elegans to generate (1) a large set of individually barcoded lineages and (2) transcriptional reporter lines from predefined promoter libraries. We find that this approach increases transformation yields up to approximately 1000-fold over current single-step methods. While we demonstrate the utility of TARDIS using C. elegans, in principle the process is adaptable to any system where experimentally generated genomic loci landing pads and diverse, heritable DNA elements can be generated.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Animals
*Caenorhabditis elegans/genetics
Transgenes
Animals, Genetically Modified
*Gene Transfer Techniques
Gene Library
RevDate: 2023-07-03
CmpDate: 2023-07-03
Is chimerism associated with cancer across the tree of life?.
PloS one, 18(6):e0287901.
Chimerism is a widespread phenomenon across the tree of life. It is defined as a multicellular organism composed of cells from other genetically distinct entities. This ability to 'tolerate' non-self cells may be linked to susceptibility to diseases like cancer. Here we test whether chimerism is associated with cancers across obligately multicellular organisms in the tree of life. We classified 12 obligately multicellular taxa from lowest to highest chimerism levels based on the existing literature on the presence of chimerism in these species. We then tested for associations of chimerism with tumour invasiveness, neoplasia (benign or malignant) prevalence and malignancy prevalence in 11 terrestrial mammalian species. We found that taxa with higher levels of chimerism have higher tumour invasiveness, though there was no association between malignancy or neoplasia and chimerism among mammals. This suggests that there may be an important biological relationship between chimerism and susceptibility to tissue invasion by cancerous cells. Studying chimerism might help us identify mechanisms underlying invasive cancers and also could provide insights into the detection and management of emerging transmissible cancers.
Additional Links: PMID-37384647
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Citation:
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@article {pmid37384647,
year = {2023},
author = {Kapsetaki, SE and Fortunato, A and Compton, Z and Rupp, SM and Nour, Z and Riggs-Davis, S and Stephenson, D and Duke, EG and Boddy, AM and Harrison, TM and Maley, CC and Aktipis, A},
title = {Is chimerism associated with cancer across the tree of life?.},
journal = {PloS one},
volume = {18},
number = {6},
pages = {e0287901},
pmid = {37384647},
issn = {1932-6203},
mesh = {Animals ; *Chimerism ; *Neoplasms/genetics ; Problem Solving ; Mammals ; },
abstract = {Chimerism is a widespread phenomenon across the tree of life. It is defined as a multicellular organism composed of cells from other genetically distinct entities. This ability to 'tolerate' non-self cells may be linked to susceptibility to diseases like cancer. Here we test whether chimerism is associated with cancers across obligately multicellular organisms in the tree of life. We classified 12 obligately multicellular taxa from lowest to highest chimerism levels based on the existing literature on the presence of chimerism in these species. We then tested for associations of chimerism with tumour invasiveness, neoplasia (benign or malignant) prevalence and malignancy prevalence in 11 terrestrial mammalian species. We found that taxa with higher levels of chimerism have higher tumour invasiveness, though there was no association between malignancy or neoplasia and chimerism among mammals. This suggests that there may be an important biological relationship between chimerism and susceptibility to tissue invasion by cancerous cells. Studying chimerism might help us identify mechanisms underlying invasive cancers and also could provide insights into the detection and management of emerging transmissible cancers.},
}
MeSH Terms:
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Animals
*Chimerism
*Neoplasms/genetics
Problem Solving
Mammals
RevDate: 2023-07-13
CmpDate: 2023-07-03
Evolution of cyclic di-GMP signalling on a short and long term time scale.
Microbiology (Reading, England), 169(6):.
Diversifying radiation of domain families within specific lineages of life indicates the importance of their functionality for the organisms. The foundation for the diversifying radiation of the cyclic di-GMP signalling network that occurred within the bacterial kingdom is most likely based in the outmost adaptability, flexibility and plasticity of the system. Integrative sensing of multiple diverse extra- and intracellular signals is made possible by the N-terminal sensory domains of the modular cyclic di-GMP turnover proteins, mutations in the protein scaffolds and subsequent signal reception by diverse receptors, which eventually rewires opposite host-associated as well as environmental life styles including parallel regulated target outputs. Natural, laboratory and microcosm derived microbial variants often with an altered multicellular biofilm behaviour as reading output demonstrated single amino acid substitutions to substantially alter catalytic activity including substrate specificity. Truncations and domain swapping of cyclic di-GMP signalling genes and horizontal gene transfer suggest rewiring of the network. Presence of cyclic di-GMP signalling genes on horizontally transferable elements in particular observed in extreme acidophilic bacteria indicates that cyclic di-GMP signalling and biofilm components are under selective pressure in these types of environments. On a short and long term evolutionary scale, within a species and in families within bacterial orders, respectively, the cyclic di-GMP signalling network can also rapidly disappear. To investigate variability of the cyclic di-GMP signalling system on various levels will give clues about evolutionary forces and discover novel physiological and metabolic pathways affected by this intriguing second messenger signalling system.
Additional Links: PMID-37384391
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Citation:
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@article {pmid37384391,
year = {2023},
author = {Römling, U and Cao, LY and Bai, FW},
title = {Evolution of cyclic di-GMP signalling on a short and long term time scale.},
journal = {Microbiology (Reading, England)},
volume = {169},
number = {6},
pages = {},
pmid = {37384391},
issn = {1465-2080},
mesh = {Humans ; *Signal Transduction ; *Second Messenger Systems ; Amino Acid Substitution ; Biofilms ; Gene Transfer, Horizontal ; },
abstract = {Diversifying radiation of domain families within specific lineages of life indicates the importance of their functionality for the organisms. The foundation for the diversifying radiation of the cyclic di-GMP signalling network that occurred within the bacterial kingdom is most likely based in the outmost adaptability, flexibility and plasticity of the system. Integrative sensing of multiple diverse extra- and intracellular signals is made possible by the N-terminal sensory domains of the modular cyclic di-GMP turnover proteins, mutations in the protein scaffolds and subsequent signal reception by diverse receptors, which eventually rewires opposite host-associated as well as environmental life styles including parallel regulated target outputs. Natural, laboratory and microcosm derived microbial variants often with an altered multicellular biofilm behaviour as reading output demonstrated single amino acid substitutions to substantially alter catalytic activity including substrate specificity. Truncations and domain swapping of cyclic di-GMP signalling genes and horizontal gene transfer suggest rewiring of the network. Presence of cyclic di-GMP signalling genes on horizontally transferable elements in particular observed in extreme acidophilic bacteria indicates that cyclic di-GMP signalling and biofilm components are under selective pressure in these types of environments. On a short and long term evolutionary scale, within a species and in families within bacterial orders, respectively, the cyclic di-GMP signalling network can also rapidly disappear. To investigate variability of the cyclic di-GMP signalling system on various levels will give clues about evolutionary forces and discover novel physiological and metabolic pathways affected by this intriguing second messenger signalling system.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Signal Transduction
*Second Messenger Systems
Amino Acid Substitution
Biofilms
Gene Transfer, Horizontal
RevDate: 2023-08-03
CmpDate: 2023-08-03
The use of tissue clearing to study renal transport mechanisms and kidney remodelling.
Current opinion in nephrology and hypertension, 32(5):458-466.
PURPOSE OF REVIEW: Tissue clearing enables examination of biological structures at subcellular resolution in three dimensions. It uncovered the spatial and temporal plasticity of multicellular kidney structures that occur during homeostatic stress. This article will review the recent development in tissue clearing protocols and how it facilitated the study of renal transport mechanisms and remodelling of the kidney.
RECENT FINDINGS: Tissue clearing methods have evolved from primarily labelling proteins in thin tissue or individual organs to visualizing both RNA and protein simultaneously in whole animals or human organs. The use of small antibody fragments and innovative imaging techniques improved immunolabelling and resolution. These advances opened up new avenues for studying organ crosstalk and diseases that affect multiple parts of the organism. Accumulating evidence suggests that tubule remodelling can occur rapidly in response to homeostatic stress or injury, allowing for adjustments in the quantitative expression of renal transporters. Tissue clearing helped to better understand the development of tubule cystogenesis, renal hypertension and salt wasting syndromes, and revealed potential progenitor cells in the kidney.
SUMMARY: The continued evolution and improvement of tissue clearing methods can help to gain deep biological insights into the structure and function of the kidney, which will have clinical implications.
Additional Links: PMID-37382119
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PubMed:
Citation:
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@article {pmid37382119,
year = {2023},
author = {Saritas, T},
title = {The use of tissue clearing to study renal transport mechanisms and kidney remodelling.},
journal = {Current opinion in nephrology and hypertension},
volume = {32},
number = {5},
pages = {458-466},
doi = {10.1097/MNH.0000000000000904},
pmid = {37382119},
issn = {1473-6543},
mesh = {Animals ; Humans ; *Imaging, Three-Dimensional/methods ; *Kidney ; },
abstract = {PURPOSE OF REVIEW: Tissue clearing enables examination of biological structures at subcellular resolution in three dimensions. It uncovered the spatial and temporal plasticity of multicellular kidney structures that occur during homeostatic stress. This article will review the recent development in tissue clearing protocols and how it facilitated the study of renal transport mechanisms and remodelling of the kidney.
RECENT FINDINGS: Tissue clearing methods have evolved from primarily labelling proteins in thin tissue or individual organs to visualizing both RNA and protein simultaneously in whole animals or human organs. The use of small antibody fragments and innovative imaging techniques improved immunolabelling and resolution. These advances opened up new avenues for studying organ crosstalk and diseases that affect multiple parts of the organism. Accumulating evidence suggests that tubule remodelling can occur rapidly in response to homeostatic stress or injury, allowing for adjustments in the quantitative expression of renal transporters. Tissue clearing helped to better understand the development of tubule cystogenesis, renal hypertension and salt wasting syndromes, and revealed potential progenitor cells in the kidney.
SUMMARY: The continued evolution and improvement of tissue clearing methods can help to gain deep biological insights into the structure and function of the kidney, which will have clinical implications.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Humans
*Imaging, Three-Dimensional/methods
*Kidney
RevDate: 2023-08-07
CmpDate: 2023-08-07
The constitutively active pSMAD2/3 relatively improves the proliferation of chicken primordial germ cells.
Molecular reproduction and development, 90(6):339-357.
In many multicellular organisms, mature gametes originate from primordial germ cells (PGCs). Improvements in the culture of PGCs are important not only for developmental biology research, but also for preserving endangered species, and for genome editing and transgenic animal technologies. SMAD2/3 appear to be powerful regulators of gene expression; however, their potential positive impact on the regulation of PGC proliferation has not been taken into consideration. Here, the effect of TGF-β signaling as the upstream activator of SMAD2/3 transcription factors was evaluated on chicken PGCs' proliferation. For this, chicken PGCs at stages 26-28 Hamburger-Hamilton were obtained from the embryonic gonadal regions and cultured on different feeders or feeder-free substrates. The results showed that TGF-β signaling agonists (IDE1 and Activin-A) improved PGC proliferation to some extent while treatment with SB431542, the antagonist of TGF-β, disrupted PGCs' proliferation. However, the transfection of PGCs with constitutively active SMAD2/3 (SMAD2/3CA) resulted in improved PGC proliferation for more than 5 weeks. The results confirmed the interactions between overexpressed SMAD2/3CA and pluripotency-associated genes NANOG, OCT4, and SOX2. According to the results, the application of SMAD2/3CA could represent a step toward achieving an efficient expansion of avian PGCs.
Additional Links: PMID-37379342
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PubMed:
Citation:
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@article {pmid37379342,
year = {2023},
author = {Zare, M and Mirhoseini, SZ and Ghovvati, S and Yakhkeshi, S and Hesaraki, M and Barati, M and Sayyahpour, FA and Baharvand, H and Hassani, SN},
title = {The constitutively active pSMAD2/3 relatively improves the proliferation of chicken primordial germ cells.},
journal = {Molecular reproduction and development},
volume = {90},
number = {6},
pages = {339-357},
doi = {10.1002/mrd.23689},
pmid = {37379342},
issn = {1098-2795},
mesh = {Animals ; *Chickens/metabolism ; *Transforming Growth Factor beta/metabolism ; Transcription Factors/metabolism ; Germ Cells ; Cell Proliferation ; Cells, Cultured ; },
abstract = {In many multicellular organisms, mature gametes originate from primordial germ cells (PGCs). Improvements in the culture of PGCs are important not only for developmental biology research, but also for preserving endangered species, and for genome editing and transgenic animal technologies. SMAD2/3 appear to be powerful regulators of gene expression; however, their potential positive impact on the regulation of PGC proliferation has not been taken into consideration. Here, the effect of TGF-β signaling as the upstream activator of SMAD2/3 transcription factors was evaluated on chicken PGCs' proliferation. For this, chicken PGCs at stages 26-28 Hamburger-Hamilton were obtained from the embryonic gonadal regions and cultured on different feeders or feeder-free substrates. The results showed that TGF-β signaling agonists (IDE1 and Activin-A) improved PGC proliferation to some extent while treatment with SB431542, the antagonist of TGF-β, disrupted PGCs' proliferation. However, the transfection of PGCs with constitutively active SMAD2/3 (SMAD2/3CA) resulted in improved PGC proliferation for more than 5 weeks. The results confirmed the interactions between overexpressed SMAD2/3CA and pluripotency-associated genes NANOG, OCT4, and SOX2. According to the results, the application of SMAD2/3CA could represent a step toward achieving an efficient expansion of avian PGCs.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Chickens/metabolism
*Transforming Growth Factor beta/metabolism
Transcription Factors/metabolism
Germ Cells
Cell Proliferation
Cells, Cultured
RevDate: 2023-07-01
Conserved organ-specific microbial assemblages in different populations of a terrestrial crab.
Frontiers in microbiology, 14:1113617.
Microorganisms are ubiquitous in the environment and provide genetic and physiological functions to multicellular organisms. Knowledge on the associated microbiota is becoming highly relevant to understand the host's ecology and biology. Among invertebrates, many examples of endosymbiosis have been described, such as those in corals, ants, and termites. At present, however, little is known on the presence, diversity, and putative roles of the microbiota associated to brachyuran crabs in relation to their environment. In this work we investigated the associated microbiota of three populations of the terrestrial brachyuran crab Chiromantes haematocheir to find evidence of a conserved organ-specific microbiome unrelated to the population of origin and dissimilar from environmental microbial assemblages. Bacterial 16S rRNA gene and fungal ITS sequences were obtained from selected crab organs and environmental matrices to profile microbial communities. Despite the presence of truly marine larval stages and the absence of a gregarious behaviour, favouring microbiota exchanges, we found common, organ-specific microbiota, associated with the gut and the gills of crabs from the different populations (with more than 15% of the genera detected specifically enriched only in one organ). These findings suggest the presence of possible functional roles of the organ-specific microbiota.
Additional Links: PMID-37378290
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Citation:
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@article {pmid37378290,
year = {2023},
author = {Bacci, G and Fratini, S and Meriggi, N and Cheng, CLY and Ng, KH and Pindo, M and Iannucci, A and Mengoni, A and Cavalieri, D and Cannicci, S},
title = {Conserved organ-specific microbial assemblages in different populations of a terrestrial crab.},
journal = {Frontiers in microbiology},
volume = {14},
number = {},
pages = {1113617},
pmid = {37378290},
issn = {1664-302X},
abstract = {Microorganisms are ubiquitous in the environment and provide genetic and physiological functions to multicellular organisms. Knowledge on the associated microbiota is becoming highly relevant to understand the host's ecology and biology. Among invertebrates, many examples of endosymbiosis have been described, such as those in corals, ants, and termites. At present, however, little is known on the presence, diversity, and putative roles of the microbiota associated to brachyuran crabs in relation to their environment. In this work we investigated the associated microbiota of three populations of the terrestrial brachyuran crab Chiromantes haematocheir to find evidence of a conserved organ-specific microbiome unrelated to the population of origin and dissimilar from environmental microbial assemblages. Bacterial 16S rRNA gene and fungal ITS sequences were obtained from selected crab organs and environmental matrices to profile microbial communities. Despite the presence of truly marine larval stages and the absence of a gregarious behaviour, favouring microbiota exchanges, we found common, organ-specific microbiota, associated with the gut and the gills of crabs from the different populations (with more than 15% of the genera detected specifically enriched only in one organ). These findings suggest the presence of possible functional roles of the organ-specific microbiota.},
}
RevDate: 2023-07-01
Evo Devo of the Vertebrates Integument.
Journal of developmental biology, 11(2):.
All living jawed vertebrates possess teeth or did so ancestrally. Integumental surface also includes the cornea. Conversely, no other anatomical feature differentiates the clades so readily as skin appendages do, multicellular glands in amphibians, hair follicle/gland complexes in mammals, feathers in birds, and the different types of scales. Tooth-like scales are characteristic of chondrichthyans, while mineralized dermal scales are characteristic of bony fishes. Corneous epidermal scales might have appeared twice, in squamates, and on feet in avian lineages, but posteriorly to feathers. In contrast to the other skin appendages, the origin of multicellular glands of amphibians has never been addressed. In the seventies, pioneering dermal-epidermal recombination between chick, mouse and lizard embryos showed that: (1) the clade type of the appendage is determined by the epidermis; (2) their morphogenesis requires two groups of dermal messages, first for primordia formation, second for appendage final architecture; (3) the early messages were conserved during amniotes evolution. Molecular biology studies that have identified the involved pathways, extending those data to teeth and dermal scales, suggest that the different vertebrate skin appendages evolved in parallel from a shared placode/dermal cells unit, present in a common toothed ancestor, c.a. 420 mya.
Additional Links: PMID-37367479
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Citation:
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@article {pmid37367479,
year = {2023},
author = {Dhouailly, D},
title = {Evo Devo of the Vertebrates Integument.},
journal = {Journal of developmental biology},
volume = {11},
number = {2},
pages = {},
pmid = {37367479},
issn = {2221-3759},
abstract = {All living jawed vertebrates possess teeth or did so ancestrally. Integumental surface also includes the cornea. Conversely, no other anatomical feature differentiates the clades so readily as skin appendages do, multicellular glands in amphibians, hair follicle/gland complexes in mammals, feathers in birds, and the different types of scales. Tooth-like scales are characteristic of chondrichthyans, while mineralized dermal scales are characteristic of bony fishes. Corneous epidermal scales might have appeared twice, in squamates, and on feet in avian lineages, but posteriorly to feathers. In contrast to the other skin appendages, the origin of multicellular glands of amphibians has never been addressed. In the seventies, pioneering dermal-epidermal recombination between chick, mouse and lizard embryos showed that: (1) the clade type of the appendage is determined by the epidermis; (2) their morphogenesis requires two groups of dermal messages, first for primordia formation, second for appendage final architecture; (3) the early messages were conserved during amniotes evolution. Molecular biology studies that have identified the involved pathways, extending those data to teeth and dermal scales, suggest that the different vertebrate skin appendages evolved in parallel from a shared placode/dermal cells unit, present in a common toothed ancestor, c.a. 420 mya.},
}
RevDate: 2023-07-01
CmpDate: 2023-06-26
m[6]A methylation reader IGF2BP2 activates endothelial cells to promote angiogenesis and metastasis of lung adenocarcinoma.
Molecular cancer, 22(1):99.
BACKGROUND: Lung adenocarcinoma (LUAD) is a common type of lung cancer with a high risk of metastasis, but the exact molecular mechanisms of metastasis are not yet understood.
METHODS: This study acquired single-cell transcriptomics profiling of 11 distal normal lung tissues, 11 primary LUAD tissues, and 4 metastatic LUAD tissues from the GSE131907 dataset. The lung multicellular ecosystems were characterized at a single-cell resolution, and the potential mechanisms underlying angiogenesis and metastasis of LUAD were explored.
RESULTS: We constructed a global single-cell landscape of 93,610 cells from primary and metastatic LUAD and found that IGF2BP2 was specifically expressed both in a LUAD cell subpopulation (termed as LUAD_IGF2BP2), and an endothelial cell subpopulation (termed as En_IGF2BP2). The LUAD_IGF2BP2 subpopulation progressively formed and dominated the ecology of metastatic LUAD during metastatic evolution. IGF2BP2 was preferentially secreted by exosomes in the LUAD_IGF2BP2 subpopulation, which was absorbed by the En_IGF2BP2 subpopulation in the tumor microenvironment. Subsequently, IGF2BP2 improved the RNA stability of FLT4 through m[6]A modification, thereby activating the PI3K-Akt signaling pathway, and eventually promoting angiogenesis and metastasis. Analysis of clinical data showed that IGF2BP2 was linked with poor overall survival and relapse-free survival for LUAD patients.
CONCLUSIONS: Overall, these findings provide a novel insight into the multicellular ecosystems of primary and metastatic LUAD, and demonstrate that a specific LUAD_IGF2BP2 subpopulation is a key orchestrator promoting angiogenesis and metastasis, with implications for the gene regulatory mechanisms of LUAD metastatic evolution, representing themselves as potential antiangiogenic targets.
Additional Links: PMID-37353784
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@article {pmid37353784,
year = {2023},
author = {Fang, H and Sun, Q and Zhou, J and Zhang, H and Song, Q and Zhang, H and Yu, G and Guo, Y and Huang, C and Mou, Y and Jia, C and Song, Y and Liu, A and Song, K and Lu, C and Tian, R and Wei, S and Yang, D and Chen, Y and Li, T and Wang, K and Yu, Y and Lv, Y and Mo, K and Sun, P and Yu, X and Song, X},
title = {m[6]A methylation reader IGF2BP2 activates endothelial cells to promote angiogenesis and metastasis of lung adenocarcinoma.},
journal = {Molecular cancer},
volume = {22},
number = {1},
pages = {99},
pmid = {37353784},
issn = {1476-4598},
support = {ts20190991//Taishan Scholars Project/ ; ZR2021MH323//The Natural Science Fund of Shandong Province grant/ ; 2022YD037//The Science and Technology Innovation Development Plan of Yantai/ ; 201909370036//China Scholarship Council/ ; 82103646//The National Natural Science Fund of China grant/ ; },
mesh = {Humans ; Methylation ; Ecosystem ; Endothelial Cells ; Phosphatidylinositol 3-Kinases ; Neoplasm Recurrence, Local ; *Adenocarcinoma of Lung/genetics ; *Lung Neoplasms/genetics ; Tumor Microenvironment ; RNA-Binding Proteins/genetics ; },
abstract = {BACKGROUND: Lung adenocarcinoma (LUAD) is a common type of lung cancer with a high risk of metastasis, but the exact molecular mechanisms of metastasis are not yet understood.
METHODS: This study acquired single-cell transcriptomics profiling of 11 distal normal lung tissues, 11 primary LUAD tissues, and 4 metastatic LUAD tissues from the GSE131907 dataset. The lung multicellular ecosystems were characterized at a single-cell resolution, and the potential mechanisms underlying angiogenesis and metastasis of LUAD were explored.
RESULTS: We constructed a global single-cell landscape of 93,610 cells from primary and metastatic LUAD and found that IGF2BP2 was specifically expressed both in a LUAD cell subpopulation (termed as LUAD_IGF2BP2), and an endothelial cell subpopulation (termed as En_IGF2BP2). The LUAD_IGF2BP2 subpopulation progressively formed and dominated the ecology of metastatic LUAD during metastatic evolution. IGF2BP2 was preferentially secreted by exosomes in the LUAD_IGF2BP2 subpopulation, which was absorbed by the En_IGF2BP2 subpopulation in the tumor microenvironment. Subsequently, IGF2BP2 improved the RNA stability of FLT4 through m[6]A modification, thereby activating the PI3K-Akt signaling pathway, and eventually promoting angiogenesis and metastasis. Analysis of clinical data showed that IGF2BP2 was linked with poor overall survival and relapse-free survival for LUAD patients.
CONCLUSIONS: Overall, these findings provide a novel insight into the multicellular ecosystems of primary and metastatic LUAD, and demonstrate that a specific LUAD_IGF2BP2 subpopulation is a key orchestrator promoting angiogenesis and metastasis, with implications for the gene regulatory mechanisms of LUAD metastatic evolution, representing themselves as potential antiangiogenic targets.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Methylation
Ecosystem
Endothelial Cells
Phosphatidylinositol 3-Kinases
Neoplasm Recurrence, Local
*Adenocarcinoma of Lung/genetics
*Lung Neoplasms/genetics
Tumor Microenvironment
RNA-Binding Proteins/genetics
RevDate: 2023-07-01
Lessons on fruiting body morphogenesis from genomes and transcriptomes of Agaricomycetes.
Studies in mycology, 104:1-85.
Fruiting bodies (sporocarps, sporophores or basidiomata) of mushroom-forming fungi (Agaricomycetes) are among the most complex structures produced by fungi. Unlike vegetative hyphae, fruiting bodies grow determinately and follow a genetically encoded developmental program that orchestrates their growth, tissue differentiation and sexual sporulation. In spite of more than a century of research, our understanding of the molecular details of fruiting body morphogenesis is still limited and a general synthesis on the genetics of this complex process is lacking. In this paper, we aim at a comprehensive identification of conserved genes related to fruiting body morphogenesis and distil novel functional hypotheses for functionally poorly characterised ones. As a result of this analysis, we report 921 conserved developmentally expressed gene families, only a few dozens of which have previously been reported to be involved in fruiting body development. Based on literature data, conserved expression patterns and functional annotations, we provide hypotheses on the potential role of these gene families in fruiting body development, yielding the most complete description of molecular processes in fruiting body morphogenesis to date. We discuss genes related to the initiation of fruiting, differentiation, growth, cell surface and cell wall, defence, transcriptional regulation as well as signal transduction. Based on these data we derive a general model of fruiting body development, which includes an early, proliferative phase that is mostly concerned with laying out the mushroom body plan (via cell division and differentiation), and a second phase of growth via cell expansion as well as meiotic events and sporulation. Altogether, our discussions cover 1 480 genes of Coprinopsis cinerea, and their orthologs in Agaricus bisporus, Cyclocybe aegerita, Armillaria ostoyae, Auriculariopsis ampla, Laccaria bicolor, Lentinula edodes, Lentinus tigrinus, Mycena kentingensis, Phanerochaete chrysosporium, Pleurotus ostreatus, and Schizophyllum commune, providing functional hypotheses for ~10 % of genes in the genomes of these species. Although experimental evidence for the role of these genes will need to be established in the future, our data provide a roadmap for guiding functional analyses of fruiting related genes in the Agaricomycetes. We anticipate that the gene compendium presented here, combined with developments in functional genomics approaches will contribute to uncovering the genetic bases of one of the most spectacular multicellular developmental processes in fungi. Citation: Nagy LG, Vonk PJ, Künzler M, Földi C, Virágh M, Ohm RA, Hennicke F, Bálint B, Csernetics Á, Hegedüs B, Hou Z, Liu XB, Nan S, M. Pareek M, Sahu N, Szathmári B, Varga T, Wu W, Yang X, Merényi Z (2023). Lessons on fruiting body morphogenesis from genomes and transcriptomes of Agaricomycetes. Studies in Mycology 104: 1-85. doi: 10.3114/sim.2022.104.01.
Additional Links: PMID-37351542
PubMed:
Citation:
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@article {pmid37351542,
year = {2023},
author = {Nagy, LG and Vonk, PJ and Künzler, M and Földi, C and Virágh, M and Ohm, RA and Hennicke, F and Bálint, B and Csernetics, Á and Hegedüs, B and Hou, Z and Liu, XB and Nan, S and Pareek, M and Sahu, N and Szathmári, B and Varga, T and Wu, H and Yang, X and Merényi, Z},
title = {Lessons on fruiting body morphogenesis from genomes and transcriptomes of Agaricomycetes.},
journal = {Studies in mycology},
volume = {104},
number = {},
pages = {1-85},
pmid = {37351542},
issn = {0166-0616},
abstract = {Fruiting bodies (sporocarps, sporophores or basidiomata) of mushroom-forming fungi (Agaricomycetes) are among the most complex structures produced by fungi. Unlike vegetative hyphae, fruiting bodies grow determinately and follow a genetically encoded developmental program that orchestrates their growth, tissue differentiation and sexual sporulation. In spite of more than a century of research, our understanding of the molecular details of fruiting body morphogenesis is still limited and a general synthesis on the genetics of this complex process is lacking. In this paper, we aim at a comprehensive identification of conserved genes related to fruiting body morphogenesis and distil novel functional hypotheses for functionally poorly characterised ones. As a result of this analysis, we report 921 conserved developmentally expressed gene families, only a few dozens of which have previously been reported to be involved in fruiting body development. Based on literature data, conserved expression patterns and functional annotations, we provide hypotheses on the potential role of these gene families in fruiting body development, yielding the most complete description of molecular processes in fruiting body morphogenesis to date. We discuss genes related to the initiation of fruiting, differentiation, growth, cell surface and cell wall, defence, transcriptional regulation as well as signal transduction. Based on these data we derive a general model of fruiting body development, which includes an early, proliferative phase that is mostly concerned with laying out the mushroom body plan (via cell division and differentiation), and a second phase of growth via cell expansion as well as meiotic events and sporulation. Altogether, our discussions cover 1 480 genes of Coprinopsis cinerea, and their orthologs in Agaricus bisporus, Cyclocybe aegerita, Armillaria ostoyae, Auriculariopsis ampla, Laccaria bicolor, Lentinula edodes, Lentinus tigrinus, Mycena kentingensis, Phanerochaete chrysosporium, Pleurotus ostreatus, and Schizophyllum commune, providing functional hypotheses for ~10 % of genes in the genomes of these species. Although experimental evidence for the role of these genes will need to be established in the future, our data provide a roadmap for guiding functional analyses of fruiting related genes in the Agaricomycetes. We anticipate that the gene compendium presented here, combined with developments in functional genomics approaches will contribute to uncovering the genetic bases of one of the most spectacular multicellular developmental processes in fungi. Citation: Nagy LG, Vonk PJ, Künzler M, Földi C, Virágh M, Ohm RA, Hennicke F, Bálint B, Csernetics Á, Hegedüs B, Hou Z, Liu XB, Nan S, M. Pareek M, Sahu N, Szathmári B, Varga T, Wu W, Yang X, Merényi Z (2023). Lessons on fruiting body morphogenesis from genomes and transcriptomes of Agaricomycetes. Studies in Mycology 104: 1-85. doi: 10.3114/sim.2022.104.01.},
}
RevDate: 2023-08-07
Genomes of fungi and relatives reveal delayed loss of ancestral gene families and evolution of key fungal traits.
Nature ecology & evolution, 7(8):1221-1231.
Fungi are ecologically important heterotrophs that have radiated into most niches on Earth and fulfil key ecological services. Despite intense interest in their origins, major genomic trends of their evolutionary route from a unicellular opisthokont ancestor to derived multicellular fungi remain poorly known. Here we provide a highly resolved genome-wide catalogue of gene family changes across fungal evolution inferred from the genomes of 123 fungi and relatives. We show that a dominant trend in early fungal evolution has been the gradual shedding of protist genes and the punctuated emergence of innovation by two main gene duplication events. We find that the gene content of non-Dikarya fungi resembles that of unicellular opisthokonts in many respects, owing to the conservation of protist genes in their genomes. The most rapidly duplicating gene groups included extracellular proteins and transcription factors, as well as ones linked to the coordination of nutrient uptake with growth, highlighting the transition to a sessile osmotrophic feeding strategy and subsequent lifestyle evolution as important elements of early fungal history. These results suggest that the genomes of pre-fungal ancestors evolved into the typical filamentous fungal genome by a combination of gradual gene loss, turnover and several large duplication events rather than by abrupt changes. Consequently, the taxonomically defined Fungi represents a genomically non-uniform assemblage of species.
Additional Links: PMID-37349567
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Citation:
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@article {pmid37349567,
year = {2023},
author = {Merényi, Z and Krizsán, K and Sahu, N and Liu, XB and Bálint, B and Stajich, JE and Spatafora, JW and Nagy, LG},
title = {Genomes of fungi and relatives reveal delayed loss of ancestral gene families and evolution of key fungal traits.},
journal = {Nature ecology & evolution},
volume = {7},
number = {8},
pages = {1221-1231},
pmid = {37349567},
issn = {2397-334X},
support = {758161//EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013))/ ; },
abstract = {Fungi are ecologically important heterotrophs that have radiated into most niches on Earth and fulfil key ecological services. Despite intense interest in their origins, major genomic trends of their evolutionary route from a unicellular opisthokont ancestor to derived multicellular fungi remain poorly known. Here we provide a highly resolved genome-wide catalogue of gene family changes across fungal evolution inferred from the genomes of 123 fungi and relatives. We show that a dominant trend in early fungal evolution has been the gradual shedding of protist genes and the punctuated emergence of innovation by two main gene duplication events. We find that the gene content of non-Dikarya fungi resembles that of unicellular opisthokonts in many respects, owing to the conservation of protist genes in their genomes. The most rapidly duplicating gene groups included extracellular proteins and transcription factors, as well as ones linked to the coordination of nutrient uptake with growth, highlighting the transition to a sessile osmotrophic feeding strategy and subsequent lifestyle evolution as important elements of early fungal history. These results suggest that the genomes of pre-fungal ancestors evolved into the typical filamentous fungal genome by a combination of gradual gene loss, turnover and several large duplication events rather than by abrupt changes. Consequently, the taxonomically defined Fungi represents a genomically non-uniform assemblage of species.},
}
RevDate: 2023-07-01
Insight into the metabolic potential and ecological function of a novel Magnetotactic Nitrospirota in coral reef habitat.
Frontiers in microbiology, 14:1182330.
Magnetotactic bacteria (MTB) within the Nitrospirota phylum play important roles in biogeochemical cycles due to their outstanding ability to biomineralize large amounts of magnetite magnetosomes and intracellular sulfur globules. For several decades, Nitrospirota MTB were believed to only live in freshwater or low-salinity environments. While this group have recently been found in marine sediments, their physiological features and ecological roles have remained unclear. In this study, we combine electron microscopy with genomics to characterize a novel population of Nitrospirota MTB in a coral reef area of the South China Sea. Both phylogenetic and genomic analyses revealed it as representative of a novel genus, named as Candidatus Magnetocorallium paracelense XS-1. The cells of XS-1 are small and vibrioid-shaped, and have bundled chains of bullet-shaped magnetite magnetosomes, sulfur globules, and cytoplasmic vacuole-like structures. Genomic analysis revealed that XS-1 has the potential to respire sulfate and nitrate, and utilize the Wood-Ljungdahl pathway for carbon fixation. XS-1 has versatile metabolic traits that make it different from freshwater Nitrospirota MTB, including Pta-ackA pathway, anaerobic sulfite reduction, and thiosulfate disproportionation. XS-1 also encodes both the cbb3-type and the aa3-type cytochrome c oxidases, which may function as respiratory energy-transducing enzymes under high oxygen conditions and anaerobic or microaerophilic conditions, respectively. XS-1 has multiple copies of circadian related genes in response to variability in coral reef habitat. Our results implied that XS-1 has a remarkable plasticity to adapt the environment and can play a beneficial role in coral reef ecosystems.
Additional Links: PMID-37342564
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Citation:
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@article {pmid37342564,
year = {2023},
author = {Zhao, Y and Zhang, W and Pan, H and Chen, J and Cui, K and Wu, LF and Lin, W and Xiao, T and Zhang, W and Liu, J},
title = {Insight into the metabolic potential and ecological function of a novel Magnetotactic Nitrospirota in coral reef habitat.},
journal = {Frontiers in microbiology},
volume = {14},
number = {},
pages = {1182330},
pmid = {37342564},
issn = {1664-302X},
abstract = {Magnetotactic bacteria (MTB) within the Nitrospirota phylum play important roles in biogeochemical cycles due to their outstanding ability to biomineralize large amounts of magnetite magnetosomes and intracellular sulfur globules. For several decades, Nitrospirota MTB were believed to only live in freshwater or low-salinity environments. While this group have recently been found in marine sediments, their physiological features and ecological roles have remained unclear. In this study, we combine electron microscopy with genomics to characterize a novel population of Nitrospirota MTB in a coral reef area of the South China Sea. Both phylogenetic and genomic analyses revealed it as representative of a novel genus, named as Candidatus Magnetocorallium paracelense XS-1. The cells of XS-1 are small and vibrioid-shaped, and have bundled chains of bullet-shaped magnetite magnetosomes, sulfur globules, and cytoplasmic vacuole-like structures. Genomic analysis revealed that XS-1 has the potential to respire sulfate and nitrate, and utilize the Wood-Ljungdahl pathway for carbon fixation. XS-1 has versatile metabolic traits that make it different from freshwater Nitrospirota MTB, including Pta-ackA pathway, anaerobic sulfite reduction, and thiosulfate disproportionation. XS-1 also encodes both the cbb3-type and the aa3-type cytochrome c oxidases, which may function as respiratory energy-transducing enzymes under high oxygen conditions and anaerobic or microaerophilic conditions, respectively. XS-1 has multiple copies of circadian related genes in response to variability in coral reef habitat. Our results implied that XS-1 has a remarkable plasticity to adapt the environment and can play a beneficial role in coral reef ecosystems.},
}
RevDate: 2023-07-01
CmpDate: 2023-06-22
Why did glutamate, GABA, and melatonin become intercellular signalling molecules in plants?.
eLife, 12:.
Intercellular signalling is an indispensable part of multicellular life. Understanding the commonalities and differences in how signalling molecules function in two remote branches of the tree of life may shed light on the reasons these molecules were originally recruited for intercellular signalling. Here we review the plant function of three highly studied animal intercellular signalling molecules, namely glutamate, γ-aminobutyric acid (GABA), and melatonin. By considering both their signalling function in plants and their broader physiological function, we suggest that molecules with an original function as key metabolites or active participants in reactive ion species scavenging have a high chance of becoming intercellular signalling molecules. Naturally, the evolution of machinery to transduce a message across the plasma membrane is necessary. This fact is demonstrated by three other well-studied animal intercellular signalling molecules, namely serotonin, dopamine, and acetylcholine, for which there is currently no evidence that they act as intercellular signalling molecules in plants.
Additional Links: PMID-37338964
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@article {pmid37338964,
year = {2023},
author = {Caspi, Y and Pantazopoulou, CK and Prompers, JJ and Pieterse, CMJ and Hulshoff Pol, H and Kajala, K},
title = {Why did glutamate, GABA, and melatonin become intercellular signalling molecules in plants?.},
journal = {eLife},
volume = {12},
number = {},
pages = {},
pmid = {37338964},
issn = {2050-084X},
mesh = {Animals ; *Melatonin/metabolism ; Glutamic Acid/metabolism ; Plants/metabolism ; gamma-Aminobutyric Acid/metabolism ; Signal Transduction ; },
abstract = {Intercellular signalling is an indispensable part of multicellular life. Understanding the commonalities and differences in how signalling molecules function in two remote branches of the tree of life may shed light on the reasons these molecules were originally recruited for intercellular signalling. Here we review the plant function of three highly studied animal intercellular signalling molecules, namely glutamate, γ-aminobutyric acid (GABA), and melatonin. By considering both their signalling function in plants and their broader physiological function, we suggest that molecules with an original function as key metabolites or active participants in reactive ion species scavenging have a high chance of becoming intercellular signalling molecules. Naturally, the evolution of machinery to transduce a message across the plasma membrane is necessary. This fact is demonstrated by three other well-studied animal intercellular signalling molecules, namely serotonin, dopamine, and acetylcholine, for which there is currently no evidence that they act as intercellular signalling molecules in plants.},
}
MeSH Terms:
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Animals
*Melatonin/metabolism
Glutamic Acid/metabolism
Plants/metabolism
gamma-Aminobutyric Acid/metabolism
Signal Transduction
RevDate: 2023-06-19
Proteostatic tuning underpins the evolution of novel multicellular traits.
bioRxiv : the preprint server for biology pii:2023.05.31.543183.
UNLABELLED: The evolution of multicellularity paved the way for the origin of complex life on Earth, but little is known about the mechanistic basis of early multicellular evolution. Here, we examine the molecular basis of multicellular adaptation in the Multicellularity Long Term Evolution Experiment (MuLTEE). We demonstrate that cellular elongation, a key adaptation underpinning increased biophysical toughness and organismal size, is convergently driven by downregulation of the chaperone Hsp90. Mechanistically, Hsp90-mediated morphogenesis operates by destabilizing the cyclin-dependent kinase Cdc28, resulting in delayed mitosis and prolonged polarized growth. Reintroduction of Hsp90 expression resulted in shortened cells that formed smaller groups with reduced multicellular fitness. Together, our results show how ancient protein folding systems can be tuned to drive rapid evolution at a new level of biological individuality by revealing novel developmental phenotypes.
ONE SENTENCE SUMMARY: Downregulation of Hsp90 decouples cell cycle progression and growth to drive the evolution of macroscopic multicellularity.
Additional Links: PMID-37333256
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Publisher:
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Citation:
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@article {pmid37333256,
year = {2023},
author = {Montrose, K and Lac, DT and Burnetti, AJ and Tong, K and Bozdag, GO and Hukkanen, M and Ratcliff, WC and Saarikangas, J},
title = {Proteostatic tuning underpins the evolution of novel multicellular traits.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2023.05.31.543183},
pmid = {37333256},
abstract = {UNLABELLED: The evolution of multicellularity paved the way for the origin of complex life on Earth, but little is known about the mechanistic basis of early multicellular evolution. Here, we examine the molecular basis of multicellular adaptation in the Multicellularity Long Term Evolution Experiment (MuLTEE). We demonstrate that cellular elongation, a key adaptation underpinning increased biophysical toughness and organismal size, is convergently driven by downregulation of the chaperone Hsp90. Mechanistically, Hsp90-mediated morphogenesis operates by destabilizing the cyclin-dependent kinase Cdc28, resulting in delayed mitosis and prolonged polarized growth. Reintroduction of Hsp90 expression resulted in shortened cells that formed smaller groups with reduced multicellular fitness. Together, our results show how ancient protein folding systems can be tuned to drive rapid evolution at a new level of biological individuality by revealing novel developmental phenotypes.
ONE SENTENCE SUMMARY: Downregulation of Hsp90 decouples cell cycle progression and growth to drive the evolution of macroscopic multicellularity.},
}
RevDate: 2023-07-01
Condition-dependent fitness effects of large synthetic chromosome amplifications.
bioRxiv : the preprint server for biology.
Whole-chromosome aneuploidy and large segmental amplifications can have devastating effects in multicellular organisms, from developmental disorders and miscarriage to cancer. Aneuploidy in single-celled organisms such as yeast also results in proliferative defects and reduced viability. Yet, paradoxically, CNVs are routinely observed in laboratory evolution experiments with microbes grown in stressful conditions. The defects associated with aneuploidy are often attributed to the imbalance of many differentially expressed genes on the affected chromosomes, with many genes each contributing incremental effects. An alternate hypothesis is that a small number of individual genes are large effect 'drivers' of these fitness changes when present in an altered copy number. To test these two views, we have employed a collection of strains bearing large chromosomal amplifications that we previously assayed in nutrient-limited chemostat competitions. In this study, we focus on conditions known to be poorly tolerated by aneuploid yeast-high temperature, treatment with the Hsp90 inhibitor radicicol, and growth in extended stationary phase. To identify potential genes with a large impact on fitness, we fit a piecewise constant model to fitness data across chromosome arms, filtering breakpoints in this model by magnitude to focus on regions with a large impact on fitness in each condition. While fitness generally decreased as the length of the amplification increased, we were able to identify 91 candidate regions that disproportionately impacted fitness when amplified. Consistent with our previous work with this strain collection, nearly all candidate regions were condition specific, with only five regions impacting fitness in multiple conditions.
Additional Links: PMID-37333112
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@article {pmid37333112,
year = {2023},
author = {Keller, A and Gao, LL and Witten, D and Dunham, MJ},
title = {Condition-dependent fitness effects of large synthetic chromosome amplifications.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {37333112},
support = {P41 GM103533/GM/NIGMS NIH HHS/United States ; R01 GM147040/GM/NIGMS NIH HHS/United States ; T32 HG000035/HG/NHGRI NIH HHS/United States ; },
abstract = {Whole-chromosome aneuploidy and large segmental amplifications can have devastating effects in multicellular organisms, from developmental disorders and miscarriage to cancer. Aneuploidy in single-celled organisms such as yeast also results in proliferative defects and reduced viability. Yet, paradoxically, CNVs are routinely observed in laboratory evolution experiments with microbes grown in stressful conditions. The defects associated with aneuploidy are often attributed to the imbalance of many differentially expressed genes on the affected chromosomes, with many genes each contributing incremental effects. An alternate hypothesis is that a small number of individual genes are large effect 'drivers' of these fitness changes when present in an altered copy number. To test these two views, we have employed a collection of strains bearing large chromosomal amplifications that we previously assayed in nutrient-limited chemostat competitions. In this study, we focus on conditions known to be poorly tolerated by aneuploid yeast-high temperature, treatment with the Hsp90 inhibitor radicicol, and growth in extended stationary phase. To identify potential genes with a large impact on fitness, we fit a piecewise constant model to fitness data across chromosome arms, filtering breakpoints in this model by magnitude to focus on regions with a large impact on fitness in each condition. While fitness generally decreased as the length of the amplification increased, we were able to identify 91 candidate regions that disproportionately impacted fitness when amplified. Consistent with our previous work with this strain collection, nearly all candidate regions were condition specific, with only five regions impacting fitness in multiple conditions.},
}
RevDate: 2023-06-19
CmpDate: 2023-06-19
Bacteria evolve macroscopic multicellularity by the genetic assimilation of phenotypically plastic cell clustering.
Nature communications, 14(1):3555.
The evolutionary transition from unicellularity to multicellularity was a key innovation in the history of life. Experimental evolution is an important tool to study the formation of undifferentiated cellular clusters, the likely first step of this transition. Although multicellularity first evolved in bacteria, previous experimental evolution research has primarily used eukaryotes. Moreover, it focuses on mutationally driven (and not environmentally induced) phenotypes. Here we show that both Gram-negative and Gram-positive bacteria exhibit phenotypically plastic (i.e., environmentally induced) cell clustering. Under high salinity, they form elongated clusters of ~ 2 cm. However, under habitual salinity, the clusters disintegrate and grow planktonically. We used experimental evolution with Escherichia coli to show that such clustering can be assimilated genetically: the evolved bacteria inherently grow as macroscopic multicellular clusters, even without environmental induction. Highly parallel mutations in genes linked to cell wall assembly formed the genomic basis of assimilated multicellularity. While the wildtype also showed cell shape plasticity across high versus low salinity, it was either assimilated or reversed after evolution. Interestingly, a single mutation could genetically assimilate multicellularity by modulating plasticity at multiple levels of organization. Taken together, we show that phenotypic plasticity can prime bacteria for evolving undifferentiated macroscopic multicellularity.
Additional Links: PMID-37322016
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Citation:
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@article {pmid37322016,
year = {2023},
author = {Chavhan, Y and Dey, S and Lind, PA},
title = {Bacteria evolve macroscopic multicellularity by the genetic assimilation of phenotypically plastic cell clustering.},
journal = {Nature communications},
volume = {14},
number = {1},
pages = {3555},
pmid = {37322016},
issn = {2041-1723},
mesh = {*Biological Evolution ; *Eukaryota ; Adaptation, Physiological ; Phenotype ; Bacteria ; },
abstract = {The evolutionary transition from unicellularity to multicellularity was a key innovation in the history of life. Experimental evolution is an important tool to study the formation of undifferentiated cellular clusters, the likely first step of this transition. Although multicellularity first evolved in bacteria, previous experimental evolution research has primarily used eukaryotes. Moreover, it focuses on mutationally driven (and not environmentally induced) phenotypes. Here we show that both Gram-negative and Gram-positive bacteria exhibit phenotypically plastic (i.e., environmentally induced) cell clustering. Under high salinity, they form elongated clusters of ~ 2 cm. However, under habitual salinity, the clusters disintegrate and grow planktonically. We used experimental evolution with Escherichia coli to show that such clustering can be assimilated genetically: the evolved bacteria inherently grow as macroscopic multicellular clusters, even without environmental induction. Highly parallel mutations in genes linked to cell wall assembly formed the genomic basis of assimilated multicellularity. While the wildtype also showed cell shape plasticity across high versus low salinity, it was either assimilated or reversed after evolution. Interestingly, a single mutation could genetically assimilate multicellularity by modulating plasticity at multiple levels of organization. Taken together, we show that phenotypic plasticity can prime bacteria for evolving undifferentiated macroscopic multicellularity.},
}
MeSH Terms:
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hide MeSH Terms
*Biological Evolution
*Eukaryota
Adaptation, Physiological
Phenotype
Bacteria
RevDate: 2023-06-28
CmpDate: 2023-06-16
Globally consistent response of plant microbiome diversity across hosts and continents to soil nutrients and herbivores.
Nature communications, 14(1):3516.
All multicellular organisms host a diverse microbiome composed of microbial pathogens, mutualists, and commensals, and changes in microbiome diversity or composition can alter host fitness and function. Nonetheless, we lack a general understanding of the drivers of microbiome diversity, in part because it is regulated by concurrent processes spanning scales from global to local. Global-scale environmental gradients can determine variation in microbiome diversity among sites, however an individual host's microbiome also may reflect its local micro-environment. We fill this knowledge gap by experimentally manipulating two potential mediators of plant microbiome diversity (soil nutrient supply and herbivore density) at 23 grassland sites spanning global-scale gradients in soil nutrients, climate, and plant biomass. Here we show that leaf-scale microbiome diversity in unmanipulated plots depended on the total microbiome diversity at each site, which was highest at sites with high soil nutrients and plant biomass. We also found that experimentally adding soil nutrients and excluding herbivores produced concordant results across sites, increasing microbiome diversity by increasing plant biomass, which created a shaded microclimate. This demonstration of consistent responses of microbiome diversity across a wide range of host species and environmental conditions suggests the possibility of a general, predictive understanding of microbiome diversity.
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@article {pmid37316485,
year = {2023},
author = {Seabloom, EW and Caldeira, MC and Davies, KF and Kinkel, L and Knops, JMH and Komatsu, KJ and MacDougall, AS and May, G and Millican, M and Moore, JL and Perez, LI and Porath-Krause, AJ and Power, SA and Prober, SM and Risch, AC and Stevens, C and Borer, ET},
title = {Globally consistent response of plant microbiome diversity across hosts and continents to soil nutrients and herbivores.},
journal = {Nature communications},
volume = {14},
number = {1},
pages = {3516},
pmid = {37316485},
issn = {2041-1723},
mesh = {*Herbivory ; Biomass ; *Microbiota ; Nutrients ; Soil ; },
abstract = {All multicellular organisms host a diverse microbiome composed of microbial pathogens, mutualists, and commensals, and changes in microbiome diversity or composition can alter host fitness and function. Nonetheless, we lack a general understanding of the drivers of microbiome diversity, in part because it is regulated by concurrent processes spanning scales from global to local. Global-scale environmental gradients can determine variation in microbiome diversity among sites, however an individual host's microbiome also may reflect its local micro-environment. We fill this knowledge gap by experimentally manipulating two potential mediators of plant microbiome diversity (soil nutrient supply and herbivore density) at 23 grassland sites spanning global-scale gradients in soil nutrients, climate, and plant biomass. Here we show that leaf-scale microbiome diversity in unmanipulated plots depended on the total microbiome diversity at each site, which was highest at sites with high soil nutrients and plant biomass. We also found that experimentally adding soil nutrients and excluding herbivores produced concordant results across sites, increasing microbiome diversity by increasing plant biomass, which created a shaded microclimate. This demonstration of consistent responses of microbiome diversity across a wide range of host species and environmental conditions suggests the possibility of a general, predictive understanding of microbiome diversity.},
}
MeSH Terms:
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*Herbivory
Biomass
*Microbiota
Nutrients
Soil
RevDate: 2023-07-18
CmpDate: 2023-07-11
Toward a Bio-Organon: A model of interdependence between energy, information and knowledge in living systems.
Bio Systems, 230:104939.
What is an organism? In the absence of a fundamental biological definition, what constitutes a living organism, whether it is a unicellular microbe, a multicellular being or a multi-organismal society, remains an open question. New models of living systems are needed to address the scale of this question, with implications for the relationship between humanity and planetary ecology. Here we develop a generic model of an organism that can be applied across multiple scales and through major evolutionary transitions to form a toolkit, or bio-organon, for theoretical studies of planetary-wide physiology. The tool identifies the following core organismic principles that cut across spatial scale: (1) evolvability through self-knowledge, (2) entanglement between energy and information, and (3) extrasomatic "technology" to scaffold increases in spatial scale. Living systems are generally defined by their ability to self-sustain against entropic forces of degradation. Life "knows" how to survive from the inside, not from its genetic code alone, but by utilizing this code through dynamically embodied and functionally specialized flows of information and energy. That is, entangled metabolic and communication networks bring encoded knowledge to life in order to sustain life. However, knowledge is itself evolved and is evolving. The functional coupling between knowledge, energy and information has ancient origins, enabling the original, cellular "biotechnology," and cumulative evolutionary creativity in biochemical products and forms. Cellular biotechnology also enabled the nesting of specialized cells into multicellular organisms. This nested organismal hierarchy can be extended further, suggesting that an organism of organisms, or a human "superorganism," is not only possible, but in keeping with evolutionary trends.
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@article {pmid37295595,
year = {2023},
author = {Jacob, MS},
title = {Toward a Bio-Organon: A model of interdependence between energy, information and knowledge in living systems.},
journal = {Bio Systems},
volume = {230},
number = {},
pages = {104939},
doi = {10.1016/j.biosystems.2023.104939},
pmid = {37295595},
issn = {1872-8324},
mesh = {Humans ; *Biological Evolution ; *Models, Theoretical ; },
abstract = {What is an organism? In the absence of a fundamental biological definition, what constitutes a living organism, whether it is a unicellular microbe, a multicellular being or a multi-organismal society, remains an open question. New models of living systems are needed to address the scale of this question, with implications for the relationship between humanity and planetary ecology. Here we develop a generic model of an organism that can be applied across multiple scales and through major evolutionary transitions to form a toolkit, or bio-organon, for theoretical studies of planetary-wide physiology. The tool identifies the following core organismic principles that cut across spatial scale: (1) evolvability through self-knowledge, (2) entanglement between energy and information, and (3) extrasomatic "technology" to scaffold increases in spatial scale. Living systems are generally defined by their ability to self-sustain against entropic forces of degradation. Life "knows" how to survive from the inside, not from its genetic code alone, but by utilizing this code through dynamically embodied and functionally specialized flows of information and energy. That is, entangled metabolic and communication networks bring encoded knowledge to life in order to sustain life. However, knowledge is itself evolved and is evolving. The functional coupling between knowledge, energy and information has ancient origins, enabling the original, cellular "biotechnology," and cumulative evolutionary creativity in biochemical products and forms. Cellular biotechnology also enabled the nesting of specialized cells into multicellular organisms. This nested organismal hierarchy can be extended further, suggesting that an organism of organisms, or a human "superorganism," is not only possible, but in keeping with evolutionary trends.},
}
MeSH Terms:
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Humans
*Biological Evolution
*Models, Theoretical
RevDate: 2023-06-15
CmpDate: 2023-06-09
Human SAMD9 is a poxvirus-activatable anticodon nuclease inhibiting codon-specific protein synthesis.
Science advances, 9(23):eadh8502.
As a defense strategy against viruses or competitors, some microbes use anticodon nucleases (ACNases) to deplete essential tRNAs, effectively halting global protein synthesis. However, this mechanism has not been observed in multicellular eukaryotes. Here, we report that human SAMD9 is an ACNase that specifically cleaves phenylalanine tRNA (tRNA[Phe]), resulting in codon-specific ribosomal pausing and stress signaling. While SAMD9 ACNase activity is normally latent in cells, it can be activated by poxvirus infection or rendered constitutively active by SAMD9 mutations associated with various human disorders, revealing tRNA[Phe] depletion as an antiviral mechanism and a pathogenic condition in SAMD9 disorders. We identified the N-terminal effector domain of SAMD9 as the ACNase, with substrate specificity primarily determined by a eukaryotic tRNA[Phe]-specific 2'-O-methylation at the wobble position, making virtually all eukaryotic tRNA[Phe] susceptible to SAMD9 cleavage. Notably, the structure and substrate specificity of SAMD9 ACNase differ from known microbial ACNases, suggesting convergent evolution of a common immune defense strategy targeting tRNAs.
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@article {pmid37285440,
year = {2023},
author = {Zhang, F and Ji, Q and Chaturvedi, J and Morales, M and Mao, Y and Meng, X and Dong, L and Deng, J and Qian, SB and Xiang, Y},
title = {Human SAMD9 is a poxvirus-activatable anticodon nuclease inhibiting codon-specific protein synthesis.},
journal = {Science advances},
volume = {9},
number = {23},
pages = {eadh8502},
pmid = {37285440},
issn = {2375-2548},
support = {R01 AI151638/AI/NIAID NIH HHS/United States ; },
mesh = {Humans ; *Anticodon/genetics ; *RNA, Transfer, Phe/genetics/metabolism ; Codon ; RNA, Transfer/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; },
abstract = {As a defense strategy against viruses or competitors, some microbes use anticodon nucleases (ACNases) to deplete essential tRNAs, effectively halting global protein synthesis. However, this mechanism has not been observed in multicellular eukaryotes. Here, we report that human SAMD9 is an ACNase that specifically cleaves phenylalanine tRNA (tRNA[Phe]), resulting in codon-specific ribosomal pausing and stress signaling. While SAMD9 ACNase activity is normally latent in cells, it can be activated by poxvirus infection or rendered constitutively active by SAMD9 mutations associated with various human disorders, revealing tRNA[Phe] depletion as an antiviral mechanism and a pathogenic condition in SAMD9 disorders. We identified the N-terminal effector domain of SAMD9 as the ACNase, with substrate specificity primarily determined by a eukaryotic tRNA[Phe]-specific 2'-O-methylation at the wobble position, making virtually all eukaryotic tRNA[Phe] susceptible to SAMD9 cleavage. Notably, the structure and substrate specificity of SAMD9 ACNase differ from known microbial ACNases, suggesting convergent evolution of a common immune defense strategy targeting tRNAs.},
}
MeSH Terms:
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Humans
*Anticodon/genetics
*RNA, Transfer, Phe/genetics/metabolism
Codon
RNA, Transfer/metabolism
Intracellular Signaling Peptides and Proteins/genetics
RevDate: 2023-06-27
CmpDate: 2023-06-20
Main Factors Shaping Amino Acid Usage Across Evolution.
Journal of molecular evolution, 91(4):382-390.
The standard genetic code determines that in most species, including viruses, there are 20 amino acids that are coded by 61 codons, while the other three codons are stop triplets. Considering the whole proteome each species features its own amino acid frequencies, given the slow rate of change, closely related species display similar GC content and amino acids usage. In contrast, distantly related species display different amino acid frequencies. Furthermore, within certain multicellular species, as mammals, intragenomic differences in the usage of amino acids are evident. In this communication, we shall summarize some of the most prominent and well-established factors that determine the differences found in the amino acid usage, both across evolution and intragenomically.
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@article {pmid37264211,
year = {2023},
author = {Lamolle, G and Simón, D and Iriarte, A and Musto, H},
title = {Main Factors Shaping Amino Acid Usage Across Evolution.},
journal = {Journal of molecular evolution},
volume = {91},
number = {4},
pages = {382-390},
pmid = {37264211},
issn = {1432-1432},
mesh = {Animals ; *Amino Acids/genetics ; Codon/genetics ; *Genetic Code ; Base Composition ; Proteome/genetics ; Evolution, Molecular ; Mammals/genetics ; },
abstract = {The standard genetic code determines that in most species, including viruses, there are 20 amino acids that are coded by 61 codons, while the other three codons are stop triplets. Considering the whole proteome each species features its own amino acid frequencies, given the slow rate of change, closely related species display similar GC content and amino acids usage. In contrast, distantly related species display different amino acid frequencies. Furthermore, within certain multicellular species, as mammals, intragenomic differences in the usage of amino acids are evident. In this communication, we shall summarize some of the most prominent and well-established factors that determine the differences found in the amino acid usage, both across evolution and intragenomically.},
}
MeSH Terms:
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Animals
*Amino Acids/genetics
Codon/genetics
*Genetic Code
Base Composition
Proteome/genetics
Evolution, Molecular
Mammals/genetics
RevDate: 2023-06-12
CmpDate: 2023-06-05
Diversity of the Pacific Ocean coral reef microbiome.
Nature communications, 14(1):3039.
Coral reefs are among the most diverse ecosystems on Earth. They support high biodiversity of multicellular organisms that strongly rely on associated microorganisms for health and nutrition. However, the extent of the coral reef microbiome diversity and its distribution at the oceanic basin-scale remains to be explored. Here, we systematically sampled 3 coral morphotypes, 2 fish species, and planktonic communities in 99 reefs from 32 islands across the Pacific Ocean, to assess reef microbiome composition and biogeography. We show a very large richness of reef microorganisms compared to other environments, which extrapolated to all fishes and corals of the Pacific, approximates the current estimated total prokaryotic diversity for the entire Earth. Microbial communities vary among and within the 3 animal biomes (coral, fish, plankton), and geographically. For corals, the cross-ocean patterns of diversity are different from those known for other multicellular organisms. Within each coral morphotype, community composition is always determined by geographic distance first, both at the island and across ocean scale, and then by environment. Our unprecedented sampling effort of coral reef microbiomes, as part of the Tara Pacific expedition, provides new insight into the global microbial diversity, the factors driving their distribution, and the biocomplexity of reef ecosystems.
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@article {pmid37264002,
year = {2023},
author = {Galand, PE and Ruscheweyh, HJ and Salazar, G and Hochart, C and Henry, N and Hume, BCC and Oliveira, PH and Perdereau, A and Labadie, K and Belser, C and Boissin, E and Romac, S and Poulain, J and Bourdin, G and Iwankow, G and Moulin, C and Armstrong, EJ and Paz-García, DA and Ziegler, M and Agostini, S and Banaigs, B and Boss, E and Bowler, C and de Vargas, C and Douville, E and Flores, M and Forcioli, D and Furla, P and Gilson, E and Lombard, F and Pesant, S and Reynaud, S and Thomas, OP and Troublé, R and Zoccola, D and Voolstra, CR and Thurber, RV and Sunagawa, S and Wincker, P and Allemand, D and Planes, S},
title = {Diversity of the Pacific Ocean coral reef microbiome.},
journal = {Nature communications},
volume = {14},
number = {1},
pages = {3039},
pmid = {37264002},
issn = {2041-1723},
mesh = {Animals ; Coral Reefs ; Pacific Ocean ; *Anthozoa ; Biodiversity ; *Microbiota ; Fishes ; Plankton ; },
abstract = {Coral reefs are among the most diverse ecosystems on Earth. They support high biodiversity of multicellular organisms that strongly rely on associated microorganisms for health and nutrition. However, the extent of the coral reef microbiome diversity and its distribution at the oceanic basin-scale remains to be explored. Here, we systematically sampled 3 coral morphotypes, 2 fish species, and planktonic communities in 99 reefs from 32 islands across the Pacific Ocean, to assess reef microbiome composition and biogeography. We show a very large richness of reef microorganisms compared to other environments, which extrapolated to all fishes and corals of the Pacific, approximates the current estimated total prokaryotic diversity for the entire Earth. Microbial communities vary among and within the 3 animal biomes (coral, fish, plankton), and geographically. For corals, the cross-ocean patterns of diversity are different from those known for other multicellular organisms. Within each coral morphotype, community composition is always determined by geographic distance first, both at the island and across ocean scale, and then by environment. Our unprecedented sampling effort of coral reef microbiomes, as part of the Tara Pacific expedition, provides new insight into the global microbial diversity, the factors driving their distribution, and the biocomplexity of reef ecosystems.},
}
MeSH Terms:
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Animals
Coral Reefs
Pacific Ocean
*Anthozoa
Biodiversity
*Microbiota
Fishes
Plankton
RevDate: 2023-06-20
CmpDate: 2023-06-15
Ulva: An emerging green seaweed model for systems biology.
Journal of phycology, 59(3):433-440.
Green seaweeds exhibit a wide range of morphologies and occupy various ecological niches, spanning from freshwater to marine and terrestrial habitats. These organisms, which predominantly belong to the class Ulvophyceae, showcase a remarkable instance of parallel evolution toward complex multicellularity and macroscopic thalli in the Viridiplantae lineage. Within the green seaweeds, several Ulva species ("sea lettuce") are model organisms for studying carbon assimilation, interactions with bacteria, life cycle progression, and morphogenesis. Ulva species are also notorious for their fast growth and capacity to dominate nutrient-rich, anthropogenically disturbed coastal ecosystems during "green tide" blooms. From an economic perspective, Ulva has garnered increasing attention as a promising feedstock for the production of food, feed, and biobased products, also as a means of removing excess nutrients from the environment. We propose that Ulva is poised to further develop as a model in green seaweed research. In this perspective, we focus explicitly on Ulva mutabilis/compressa as a model species and highlight the molecular data and tools that are currently available or in development. We discuss several areas that will benefit from future research or where exciting new developments have been reported in other Ulva species.
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@article {pmid37256696,
year = {2023},
author = {Blomme, J and Wichard, T and Jacobs, TB and De Clerck, O},
title = {Ulva: An emerging green seaweed model for systems biology.},
journal = {Journal of phycology},
volume = {59},
number = {3},
pages = {433-440},
doi = {10.1111/jpy.13341},
pmid = {37256696},
issn = {1529-8817},
mesh = {*Ulva ; *Seaweed ; Ecosystem ; Systems Biology ; *Chlorophyta ; },
abstract = {Green seaweeds exhibit a wide range of morphologies and occupy various ecological niches, spanning from freshwater to marine and terrestrial habitats. These organisms, which predominantly belong to the class Ulvophyceae, showcase a remarkable instance of parallel evolution toward complex multicellularity and macroscopic thalli in the Viridiplantae lineage. Within the green seaweeds, several Ulva species ("sea lettuce") are model organisms for studying carbon assimilation, interactions with bacteria, life cycle progression, and morphogenesis. Ulva species are also notorious for their fast growth and capacity to dominate nutrient-rich, anthropogenically disturbed coastal ecosystems during "green tide" blooms. From an economic perspective, Ulva has garnered increasing attention as a promising feedstock for the production of food, feed, and biobased products, also as a means of removing excess nutrients from the environment. We propose that Ulva is poised to further develop as a model in green seaweed research. In this perspective, we focus explicitly on Ulva mutabilis/compressa as a model species and highlight the molecular data and tools that are currently available or in development. We discuss several areas that will benefit from future research or where exciting new developments have been reported in other Ulva species.},
}
MeSH Terms:
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*Ulva
*Seaweed
Ecosystem
Systems Biology
*Chlorophyta
RevDate: 2023-07-04
CmpDate: 2023-06-07
The effect of mutational robustness on the evolvability of multicellular organisms and eukaryotic cells.
Journal of evolutionary biology, 36(6):906-924.
Canalization involves mutational robustness, the lack of phenotypic change as a result of genetic mutations. Given the large divergence in phenotype across species, understanding the relationship between high robustness and evolvability has been of interest to both theorists and experimentalists. Although canalization was originally proposed in the context of multicellular organisms, the effect of multicellularity and other classes of hierarchical organization on evolvability has not been considered by theoreticians. We address this issue using a Boolean population model with explicit representation of an environment in which individuals with explicit genotype and a hierarchical phenotype representing multicellularity evolve. Robustness is described by a single real number between zero and one which emerges from the genotype-phenotype map. We find that high robustness is favoured in constant environments, and lower robustness is favoured after environmental change. Multicellularity and hierarchical organization severely constrain robustness: peak evolvability occurs at an absolute level of robustness of about 0.99 compared with values of about 0.5 in a classical neutral network model. These constraints result in a sharp peak of evolvability in which the maximum is set by the fact that the fixation of adaptive mutations becomes more improbable as robustness decreases. When robustness is put under genetic control, robustness levels leading to maximum evolvability are selected for, but maximal relative fitness appears to require recombination.
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@article {pmid37256290,
year = {2023},
author = {Jiang, P and Kreitman, M and Reinitz, J},
title = {The effect of mutational robustness on the evolvability of multicellular organisms and eukaryotic cells.},
journal = {Journal of evolutionary biology},
volume = {36},
number = {6},
pages = {906-924},
pmid = {37256290},
issn = {1420-9101},
support = {R01 OD010936/OD/NIH HHS/United States ; },
mesh = {*Evolution, Molecular ; *Eukaryotic Cells ; Models, Genetic ; Mutation ; Phenotype ; },
abstract = {Canalization involves mutational robustness, the lack of phenotypic change as a result of genetic mutations. Given the large divergence in phenotype across species, understanding the relationship between high robustness and evolvability has been of interest to both theorists and experimentalists. Although canalization was originally proposed in the context of multicellular organisms, the effect of multicellularity and other classes of hierarchical organization on evolvability has not been considered by theoreticians. We address this issue using a Boolean population model with explicit representation of an environment in which individuals with explicit genotype and a hierarchical phenotype representing multicellularity evolve. Robustness is described by a single real number between zero and one which emerges from the genotype-phenotype map. We find that high robustness is favoured in constant environments, and lower robustness is favoured after environmental change. Multicellularity and hierarchical organization severely constrain robustness: peak evolvability occurs at an absolute level of robustness of about 0.99 compared with values of about 0.5 in a classical neutral network model. These constraints result in a sharp peak of evolvability in which the maximum is set by the fact that the fixation of adaptive mutations becomes more improbable as robustness decreases. When robustness is put under genetic control, robustness levels leading to maximum evolvability are selected for, but maximal relative fitness appears to require recombination.},
}
MeSH Terms:
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*Evolution, Molecular
*Eukaryotic Cells
Models, Genetic
Mutation
Phenotype
RevDate: 2023-07-18
CmpDate: 2023-07-07
Tissue Specificity of DNA Damage and Repair.
Physiology (Bethesda, Md.), 38(5):0.
DNA is a remarkable biochemical macromolecule tasked with storing the genetic information that instructs life on planet Earth. However, its inherent chemical instability within the cellular milieu is incompatible with the accurate transmission of genetic information to subsequent generations. Therefore, biochemical pathways that continuously survey and repair DNA are essential to sustain life, and the fundamental mechanisms by which different DNA lesions are repaired have remained well conserved throughout evolution. Nonetheless, the emergence of multicellular organisms led to profound differences in cellular context and physiology, leading to large variations in the predominant sources of DNA damage between different cell types and in the relative contribution of different DNA repair pathways toward genome maintenance in different tissues. While we continue to make large strides into understanding how individual DNA repair mechanisms operate on a molecular level, much less attention is given to these cell type-specific differences. This short review aims to provide a broad overview of DNA damage and repair mechanisms to nonspecialists and to highlight some fundamental open questions in tissue and cell-type-specificity of these processes, which may have profound implications for our understanding of important pathophysiological processes such as cancer, neurodegeneration, and aging.
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@article {pmid37253212,
year = {2023},
author = {Hoch, NC},
title = {Tissue Specificity of DNA Damage and Repair.},
journal = {Physiology (Bethesda, Md.)},
volume = {38},
number = {5},
pages = {0},
doi = {10.1152/physiol.00006.2023},
pmid = {37253212},
issn = {1548-9221},
mesh = {Humans ; Organ Specificity ; *DNA Damage ; *DNA Repair ; Aging/genetics ; DNA/genetics/metabolism ; },
abstract = {DNA is a remarkable biochemical macromolecule tasked with storing the genetic information that instructs life on planet Earth. However, its inherent chemical instability within the cellular milieu is incompatible with the accurate transmission of genetic information to subsequent generations. Therefore, biochemical pathways that continuously survey and repair DNA are essential to sustain life, and the fundamental mechanisms by which different DNA lesions are repaired have remained well conserved throughout evolution. Nonetheless, the emergence of multicellular organisms led to profound differences in cellular context and physiology, leading to large variations in the predominant sources of DNA damage between different cell types and in the relative contribution of different DNA repair pathways toward genome maintenance in different tissues. While we continue to make large strides into understanding how individual DNA repair mechanisms operate on a molecular level, much less attention is given to these cell type-specific differences. This short review aims to provide a broad overview of DNA damage and repair mechanisms to nonspecialists and to highlight some fundamental open questions in tissue and cell-type-specificity of these processes, which may have profound implications for our understanding of important pathophysiological processes such as cancer, neurodegeneration, and aging.},
}
MeSH Terms:
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Humans
Organ Specificity
*DNA Damage
*DNA Repair
Aging/genetics
DNA/genetics/metabolism
RevDate: 2023-06-21
CmpDate: 2023-05-31
Green land: Multiple perspectives on green algal evolution and the earliest land plants.
American journal of botany, 110(5):e16175.
Green plants, broadly defined as green algae and the land plants (together, Viridiplantae), constitute the primary eukaryotic lineage that successfully colonized Earth's emergent landscape. Members of various clades of green plants have independently made the transition from fully aquatic to subaerial habitats many times throughout Earth's history. The transition, from unicells or simple filaments to complex multicellular plant bodies with functionally differentiated tissues and organs, was accompanied by innovations built upon a genetic and phenotypic toolkit that have served aquatic green phototrophs successfully for at least a billion years. These innovations opened an enormous array of new, drier places to live on the planet and resulted in a huge diversity of land plants that have dominated terrestrial ecosystems over the past 500 million years. This review examines the greening of the land from several perspectives, from paleontology to phylogenomics, to water stress responses and the genetic toolkit shared by green algae and plants, to the genomic evolution of the sporophyte generation. We summarize advances on disparate fronts in elucidating this important event in the evolution of the biosphere and the lacunae in our understanding of it. We present the process not as a step-by-step advancement from primitive green cells to an inevitable success of embryophytes, but rather as a process of adaptations and exaptations that allowed multiple clades of green plants, with various combinations of morphological and physiological terrestrialized traits, to become diverse and successful inhabitants of the land habitats of Earth.
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@article {pmid37247371,
year = {2023},
author = {McCourt, RM and Lewis, LA and Strother, PK and Delwiche, CF and Wickett, NJ and de Vries, J and Bowman, JL},
title = {Green land: Multiple perspectives on green algal evolution and the earliest land plants.},
journal = {American journal of botany},
volume = {110},
number = {5},
pages = {e16175},
doi = {10.1002/ajb2.16175},
pmid = {37247371},
issn = {1537-2197},
mesh = {Biological Evolution ; Ecosystem ; *Embryophyta/genetics ; Phylogeny ; Plants/genetics ; *Chlorophyta/genetics ; Evolution, Molecular ; },
abstract = {Green plants, broadly defined as green algae and the land plants (together, Viridiplantae), constitute the primary eukaryotic lineage that successfully colonized Earth's emergent landscape. Members of various clades of green plants have independently made the transition from fully aquatic to subaerial habitats many times throughout Earth's history. The transition, from unicells or simple filaments to complex multicellular plant bodies with functionally differentiated tissues and organs, was accompanied by innovations built upon a genetic and phenotypic toolkit that have served aquatic green phototrophs successfully for at least a billion years. These innovations opened an enormous array of new, drier places to live on the planet and resulted in a huge diversity of land plants that have dominated terrestrial ecosystems over the past 500 million years. This review examines the greening of the land from several perspectives, from paleontology to phylogenomics, to water stress responses and the genetic toolkit shared by green algae and plants, to the genomic evolution of the sporophyte generation. We summarize advances on disparate fronts in elucidating this important event in the evolution of the biosphere and the lacunae in our understanding of it. We present the process not as a step-by-step advancement from primitive green cells to an inevitable success of embryophytes, but rather as a process of adaptations and exaptations that allowed multiple clades of green plants, with various combinations of morphological and physiological terrestrialized traits, to become diverse and successful inhabitants of the land habitats of Earth.},
}
MeSH Terms:
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Biological Evolution
Ecosystem
*Embryophyta/genetics
Phylogeny
Plants/genetics
*Chlorophyta/genetics
Evolution, Molecular
RevDate: 2023-05-29
CmpDate: 2023-05-29
Carcino-Evo-Devo, A Theory of the Evolutionary Role of Hereditary Tumors.
International journal of molecular sciences, 24(10):.
A theory of the evolutionary role of hereditary tumors, or the carcino-evo-devo theory, is being developed. The main hypothesis of the theory, the hypothesis of evolution by tumor neofunctionalization, posits that hereditary tumors provided additional cell masses during the evolution of multicellular organisms for the expression of evolutionarily novel genes. The carcino-evo-devo theory has formulated several nontrivial predictions that have been confirmed in the laboratory of the author. It also suggests several nontrivial explanations of biological phenomena previously unexplained by the existing theories or incompletely understood. By considering three major types of biological development-individual, evolutionary, and neoplastic development-within one theoretical framework, the carcino-evo-devo theory has the potential to become a unifying biological theory.
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@article {pmid37239953,
year = {2023},
author = {Kozlov, AP},
title = {Carcino-Evo-Devo, A Theory of the Evolutionary Role of Hereditary Tumors.},
journal = {International journal of molecular sciences},
volume = {24},
number = {10},
pages = {},
pmid = {37239953},
issn = {1422-0067},
support = {The strategic academic leadership program 'Priority 2030' (Agreement 075-15-2021-1333 dated 30 September 2021)//Ministry of Science and Higher Education of the Russian Federation/ ; },
mesh = {*Biological Evolution ; *Developmental Biology ; },
abstract = {A theory of the evolutionary role of hereditary tumors, or the carcino-evo-devo theory, is being developed. The main hypothesis of the theory, the hypothesis of evolution by tumor neofunctionalization, posits that hereditary tumors provided additional cell masses during the evolution of multicellular organisms for the expression of evolutionarily novel genes. The carcino-evo-devo theory has formulated several nontrivial predictions that have been confirmed in the laboratory of the author. It also suggests several nontrivial explanations of biological phenomena previously unexplained by the existing theories or incompletely understood. By considering three major types of biological development-individual, evolutionary, and neoplastic development-within one theoretical framework, the carcino-evo-devo theory has the potential to become a unifying biological theory.},
}
MeSH Terms:
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*Biological Evolution
*Developmental Biology
RevDate: 2023-05-26
Innovative insights into extrachromosomal circular DNAs in gynecologic tumors and reproduction.
Protein & cell pii:7180341 [Epub ahead of print].
Originating but free from chromosomal DNA, extrachromosomal circular DNAs (eccDNAs) are organized in circular form and have long been found in unicellular and multicellular eukaryotes. Their biogenesis and function are poorly understood as they are characterized by sequence homology with linear DNA, for which few detection methods are available. Recent advances in high-throughput sequencing technologies have revealed that eccDNAs play crucial roles in tumor formation, evolution, and drug resistance as well as aging, genomic diversity, and other biological processes, bringing it back to the research hotspot. Several mechanisms of eccDNA formation have been proposed, including the breakage-fusion-bridge (BFB) and translocation-deletion-amplification models. Gynecologic tumors and disorders of embryonic and fetal development are major threats to human reproductive health. The roles of eccDNAs in these pathological processes have been partially elucidated since the first discovery of eccDNA in pig sperm and the double minutes in ovarian cancer ascites. The present review summarized the research history, biogenesis, and currently available detection and analytical methods for eccDNAs and clarified their functions in gynecologic tumors and reproduction. We also proposed the application of eccDNAs as drug targets and liquid biopsy markers for prenatal diagnosis and the early detection, prognosis, and treatment of gynecologic tumors. This review lays theoretical foundations for future investigations into the complex regulatory networks of eccDNAs in vital physiological and pathological processes.
Additional Links: PMID-37233789
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@article {pmid37233789,
year = {2023},
author = {Wu, N and Wei, L and Zhu, Z and Liu, Q and Li, K and Mao, F and Qiao, J and Zhao, X},
title = {Innovative insights into extrachromosomal circular DNAs in gynecologic tumors and reproduction.},
journal = {Protein & cell},
volume = {},
number = {},
pages = {},
doi = {10.1093/procel/pwad032},
pmid = {37233789},
issn = {1674-8018},
abstract = {Originating but free from chromosomal DNA, extrachromosomal circular DNAs (eccDNAs) are organized in circular form and have long been found in unicellular and multicellular eukaryotes. Their biogenesis and function are poorly understood as they are characterized by sequence homology with linear DNA, for which few detection methods are available. Recent advances in high-throughput sequencing technologies have revealed that eccDNAs play crucial roles in tumor formation, evolution, and drug resistance as well as aging, genomic diversity, and other biological processes, bringing it back to the research hotspot. Several mechanisms of eccDNA formation have been proposed, including the breakage-fusion-bridge (BFB) and translocation-deletion-amplification models. Gynecologic tumors and disorders of embryonic and fetal development are major threats to human reproductive health. The roles of eccDNAs in these pathological processes have been partially elucidated since the first discovery of eccDNA in pig sperm and the double minutes in ovarian cancer ascites. The present review summarized the research history, biogenesis, and currently available detection and analytical methods for eccDNAs and clarified their functions in gynecologic tumors and reproduction. We also proposed the application of eccDNAs as drug targets and liquid biopsy markers for prenatal diagnosis and the early detection, prognosis, and treatment of gynecologic tumors. This review lays theoretical foundations for future investigations into the complex regulatory networks of eccDNAs in vital physiological and pathological processes.},
}
RevDate: 2023-05-29
Temperature-Promoted Giant Unilamellar Vesicle (GUV) Aggregation: A Way of Multicellular Formation.
Current issues in molecular biology, 45(5):3757-3771.
The evolution of unicellular to multicellular life is considered to be an important step in the origin of life, and it is crucial to study the influence of environmental factors on this process through cell models in the laboratory. In this paper, we used giant unilamellar vesicles (GUVs) as a cell model to investigate the relationship between environmental temperature changes and the evolution of unicellular to multicellular life. The zeta potential of GUVs and the conformation of the headgroup of phospholipid molecules at different temperatures were examined using phase analysis light scattering (PALS) and attenuated total reflection-Fourier transform infrared spectroscopy (ATR-FTIR), respectively. In addition, the effect of increasing temperature on the aggregation of GUVs was further investigated in ionic solutions, and the possible mechanisms involved were explored. The results showed that increasing temperature reduced the repulsive forces between cells models and promoted their aggregation. This study could effectively contribute to our understanding of the evolution of primitive unicellular to multicellular life.
Additional Links: PMID-37232711
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Citation:
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@article {pmid37232711,
year = {2023},
author = {Wang, X and Zhang, Y and Xie, M and Wang, Z and Qiao, H},
title = {Temperature-Promoted Giant Unilamellar Vesicle (GUV) Aggregation: A Way of Multicellular Formation.},
journal = {Current issues in molecular biology},
volume = {45},
number = {5},
pages = {3757-3771},
pmid = {37232711},
issn = {1467-3045},
support = {Grant No. cstc2021jcyj-msxmX0550//General Project of Chongqing Natural Science Foundation/ ; },
abstract = {The evolution of unicellular to multicellular life is considered to be an important step in the origin of life, and it is crucial to study the influence of environmental factors on this process through cell models in the laboratory. In this paper, we used giant unilamellar vesicles (GUVs) as a cell model to investigate the relationship between environmental temperature changes and the evolution of unicellular to multicellular life. The zeta potential of GUVs and the conformation of the headgroup of phospholipid molecules at different temperatures were examined using phase analysis light scattering (PALS) and attenuated total reflection-Fourier transform infrared spectroscopy (ATR-FTIR), respectively. In addition, the effect of increasing temperature on the aggregation of GUVs was further investigated in ionic solutions, and the possible mechanisms involved were explored. The results showed that increasing temperature reduced the repulsive forces between cells models and promoted their aggregation. This study could effectively contribute to our understanding of the evolution of primitive unicellular to multicellular life.},
}
RevDate: 2023-05-25
Recent advances and perspectives in nucleotide second messenger signaling in bacteria.
microLife, 4:uqad015.
Nucleotide second messengers act as intracellular 'secondary' signals that represent environmental or cellular cues, i.e. the 'primary' signals. As such, they are linking sensory input with regulatory output in all living cells. The amazing physiological versatility, the mechanistic diversity of second messenger synthesis, degradation, and action as well as the high level of integration of second messenger pathways and networks in prokaryotes has only recently become apparent. In these networks, specific second messengers play conserved general roles. Thus, (p)ppGpp coordinates growth and survival in response to nutrient availability and various stresses, while c-di-GMP is the nucleotide signaling molecule to orchestrate bacterial adhesion and multicellularity. c-di-AMP links osmotic balance and metabolism and that it does so even in Archaea may suggest a very early evolutionary origin of second messenger signaling. Many of the enzymes that make or break second messengers show complex sensory domain architectures, which allow multisignal integration. The multiplicity of c-di-GMP-related enzymes in many species has led to the discovery that bacterial cells are even able to use the same freely diffusible second messenger in local signaling pathways that can act in parallel without cross-talking. On the other hand, signaling pathways operating with different nucleotides can intersect in elaborate signaling networks. Apart from the small number of common signaling nucleotides that bacteria use for controlling their cellular "business," diverse nucleotides were recently found to play very specific roles in phage defense. Furthermore, these systems represent the phylogenetic ancestors of cyclic nucleotide-activated immune signaling in eukaryotes.
Additional Links: PMID-37223732
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@article {pmid37223732,
year = {2023},
author = {Hengge, R and Pruteanu, M and Stülke, J and Tschowri, N and Turgay, K},
title = {Recent advances and perspectives in nucleotide second messenger signaling in bacteria.},
journal = {microLife},
volume = {4},
number = {},
pages = {uqad015},
pmid = {37223732},
issn = {2633-6693},
abstract = {Nucleotide second messengers act as intracellular 'secondary' signals that represent environmental or cellular cues, i.e. the 'primary' signals. As such, they are linking sensory input with regulatory output in all living cells. The amazing physiological versatility, the mechanistic diversity of second messenger synthesis, degradation, and action as well as the high level of integration of second messenger pathways and networks in prokaryotes has only recently become apparent. In these networks, specific second messengers play conserved general roles. Thus, (p)ppGpp coordinates growth and survival in response to nutrient availability and various stresses, while c-di-GMP is the nucleotide signaling molecule to orchestrate bacterial adhesion and multicellularity. c-di-AMP links osmotic balance and metabolism and that it does so even in Archaea may suggest a very early evolutionary origin of second messenger signaling. Many of the enzymes that make or break second messengers show complex sensory domain architectures, which allow multisignal integration. The multiplicity of c-di-GMP-related enzymes in many species has led to the discovery that bacterial cells are even able to use the same freely diffusible second messenger in local signaling pathways that can act in parallel without cross-talking. On the other hand, signaling pathways operating with different nucleotides can intersect in elaborate signaling networks. Apart from the small number of common signaling nucleotides that bacteria use for controlling their cellular "business," diverse nucleotides were recently found to play very specific roles in phage defense. Furthermore, these systems represent the phylogenetic ancestors of cyclic nucleotide-activated immune signaling in eukaryotes.},
}
RevDate: 2023-06-13
CmpDate: 2023-05-25
Pervasive mRNA uridylation in fission yeast is catalysed by both Cid1 and Cid16 terminal uridyltransferases.
PloS one, 18(5):e0285576.
Messenger RNA uridylation is pervasive and conserved among eukaryotes, but the consequences of this modification for mRNA fate are still under debate. Utilising a simple model organism to study uridylation may facilitate efforts to understand the cellular function of this process. Here we demonstrate that uridylation can be detected using simple bioinformatics approach. We utilise it to unravel widespread transcript uridylation in fission yeast and demonstrate the contribution of both Cid1 and Cid16, the only two annotated terminal uridyltransferases (TUT-ases) in this yeast. To detect uridylation in transcriptome data, we used a RNA-sequencing (RNA-seq) library preparation protocol involving initial linker ligation to fragmented RNA-an approach borrowed from small RNA sequencing that was commonly used in older RNA-seq protocols. We next explored the data to detect uridylation marks. Our analysis show that uridylation in yeast is pervasive, similarly to the one in multicellular organisms. Importantly, our results confirm the role of the cytoplasmic uridyltransferase Cid1 as the primary uridylation catalyst. However, we also observed an auxiliary role of the second uridyltransferase, Cid16. Thus both fission yeast uridyltransferases are involved in mRNA uridylation. Intriguingly, we found no physiological phenotype of the single and double deletion mutants of cid1 and cid16 and only minimal impact of uridylation on steady-state mRNA levels. Our work establishes fission yeast as a potent model to study uridylation in a simple eukaryote, and we demonstrate that it is possible to detect uridylation marks in RNA-seq data without the need for specific methodologies.
Additional Links: PMID-37220133
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@article {pmid37220133,
year = {2023},
author = {Lipińska-Zubrycka, L and Grochowski, M and Bähler, J and Małecki, M},
title = {Pervasive mRNA uridylation in fission yeast is catalysed by both Cid1 and Cid16 terminal uridyltransferases.},
journal = {PloS one},
volume = {18},
number = {5},
pages = {e0285576},
pmid = {37220133},
issn = {1932-6203},
support = {095598/Z/11/Z/WT_/Wellcome Trust/United Kingdom ; },
mesh = {RNA, Messenger ; *Schizosaccharomyces ; Saccharomyces cerevisiae ; RNA ; Catalysis ; UDPglucose-Hexose-1-Phosphate Uridylyltransferase ; Nucleotidyltransferases ; *Schizosaccharomyces pombe Proteins ; },
abstract = {Messenger RNA uridylation is pervasive and conserved among eukaryotes, but the consequences of this modification for mRNA fate are still under debate. Utilising a simple model organism to study uridylation may facilitate efforts to understand the cellular function of this process. Here we demonstrate that uridylation can be detected using simple bioinformatics approach. We utilise it to unravel widespread transcript uridylation in fission yeast and demonstrate the contribution of both Cid1 and Cid16, the only two annotated terminal uridyltransferases (TUT-ases) in this yeast. To detect uridylation in transcriptome data, we used a RNA-sequencing (RNA-seq) library preparation protocol involving initial linker ligation to fragmented RNA-an approach borrowed from small RNA sequencing that was commonly used in older RNA-seq protocols. We next explored the data to detect uridylation marks. Our analysis show that uridylation in yeast is pervasive, similarly to the one in multicellular organisms. Importantly, our results confirm the role of the cytoplasmic uridyltransferase Cid1 as the primary uridylation catalyst. However, we also observed an auxiliary role of the second uridyltransferase, Cid16. Thus both fission yeast uridyltransferases are involved in mRNA uridylation. Intriguingly, we found no physiological phenotype of the single and double deletion mutants of cid1 and cid16 and only minimal impact of uridylation on steady-state mRNA levels. Our work establishes fission yeast as a potent model to study uridylation in a simple eukaryote, and we demonstrate that it is possible to detect uridylation marks in RNA-seq data without the need for specific methodologies.},
}
MeSH Terms:
show MeSH Terms
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RNA, Messenger
*Schizosaccharomyces
Saccharomyces cerevisiae
RNA
Catalysis
UDPglucose-Hexose-1-Phosphate Uridylyltransferase
Nucleotidyltransferases
*Schizosaccharomyces pombe Proteins
RevDate: 2023-07-01
CmpDate: 2023-06-26
Genomes comparison of two Proteus mirabilis clones showing varied swarming ability.
Molecular biology reports, 50(7):5817-5826.
BACKGROUND: Proteus mirabilis is a Gram-negative bacteria most noted for its involvement with catheter-associated urinary tract infections. It is also known for its multicellular migration over solid surfaces, referred to as 'swarming motility'. Here we analyzed the genomic sequences of two P. mirabilis isolates, designated K38 and K39, which exhibit varied swarming ability.
METHODS AND RESULTS: The isolates genomes were sequenced using Illumina NextSeq sequencer, resulting in about 3.94 Mbp, with a GC content of 38.6%, genomes. Genomes were subjected for in silico comparative investigation. We revealed that, despite a difference in swarming motility, the isolates showed high genomic relatedness (up to 100% ANI similarity), suggesting that one of the isolates probably originated from the other.
CONCLUSIONS: The genomic sequences will allow us to investigate the mechanism driving this intriguing phenotypic heterogeneity between closely related P. mirabilis isolates. Phenotypic heterogeneity is an adaptive strategy of bacterial cells to several environmental pressures. It is also an important factor related to their pathogenesis. Therefore, the availability of these genomic sequences will facilitate studies that focus on the host-pathogen interactions during catheter-associated urinary tract infections.
Additional Links: PMID-37219671
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Citation:
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@article {pmid37219671,
year = {2023},
author = {Gmiter, D and Pacak, I and Nawrot, S and Czerwonka, G and Kaca, W},
title = {Genomes comparison of two Proteus mirabilis clones showing varied swarming ability.},
journal = {Molecular biology reports},
volume = {50},
number = {7},
pages = {5817-5826},
pmid = {37219671},
issn = {1573-4978},
support = {2019/33/N/NZ6/02406//Narodowym Centrum Nauki/ ; 2017/01/X/NZ6/01141//Narodowe Centrum Nauki/ ; },
mesh = {Humans ; Proteus mirabilis/genetics ; *Urinary Tract Infections/genetics/microbiology ; Clone Cells ; *Proteus Infections/microbiology ; },
abstract = {BACKGROUND: Proteus mirabilis is a Gram-negative bacteria most noted for its involvement with catheter-associated urinary tract infections. It is also known for its multicellular migration over solid surfaces, referred to as 'swarming motility'. Here we analyzed the genomic sequences of two P. mirabilis isolates, designated K38 and K39, which exhibit varied swarming ability.
METHODS AND RESULTS: The isolates genomes were sequenced using Illumina NextSeq sequencer, resulting in about 3.94 Mbp, with a GC content of 38.6%, genomes. Genomes were subjected for in silico comparative investigation. We revealed that, despite a difference in swarming motility, the isolates showed high genomic relatedness (up to 100% ANI similarity), suggesting that one of the isolates probably originated from the other.
CONCLUSIONS: The genomic sequences will allow us to investigate the mechanism driving this intriguing phenotypic heterogeneity between closely related P. mirabilis isolates. Phenotypic heterogeneity is an adaptive strategy of bacterial cells to several environmental pressures. It is also an important factor related to their pathogenesis. Therefore, the availability of these genomic sequences will facilitate studies that focus on the host-pathogen interactions during catheter-associated urinary tract infections.},
}
MeSH Terms:
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Humans
Proteus mirabilis/genetics
*Urinary Tract Infections/genetics/microbiology
Clone Cells
*Proteus Infections/microbiology
RevDate: 2023-06-15
CmpDate: 2023-06-15
Regulative development as a model for origin of life and artificial life studies.
Bio Systems, 229:104927.
Using the formal framework of the Free Energy Principle, we show how generic thermodynamic requirements on bidirectional information exchange between a system and its environment can generate complexity. This leads to the emergence of hierarchical computational architectures in systems that operate sufficiently far from thermal equilibrium. In this setting, the environment of any system increases its ability to predict system behavior by "engineering" the system towards increased morphological complexity and hence larger-scale, more macroscopic behaviors. When seen in this light, regulative development becomes an environmentally-driven process in which "parts" are assembled to produce a system with predictable behavior. We suggest on this basis that life is thermodynamically favorable and that, when designing artificial living systems, human engineers are acting like a generic "environment".
Additional Links: PMID-37211257
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@article {pmid37211257,
year = {2023},
author = {Fields, C and Levin, M},
title = {Regulative development as a model for origin of life and artificial life studies.},
journal = {Bio Systems},
volume = {229},
number = {},
pages = {104927},
doi = {10.1016/j.biosystems.2023.104927},
pmid = {37211257},
issn = {1872-8324},
mesh = {Humans ; *Artificial Life ; Thermodynamics ; },
abstract = {Using the formal framework of the Free Energy Principle, we show how generic thermodynamic requirements on bidirectional information exchange between a system and its environment can generate complexity. This leads to the emergence of hierarchical computational architectures in systems that operate sufficiently far from thermal equilibrium. In this setting, the environment of any system increases its ability to predict system behavior by "engineering" the system towards increased morphological complexity and hence larger-scale, more macroscopic behaviors. When seen in this light, regulative development becomes an environmentally-driven process in which "parts" are assembled to produce a system with predictable behavior. We suggest on this basis that life is thermodynamically favorable and that, when designing artificial living systems, human engineers are acting like a generic "environment".},
}
MeSH Terms:
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Humans
*Artificial Life
Thermodynamics
RevDate: 2023-06-01
CmpDate: 2023-06-01
Single Exosome Amperometric Measurements Reveal Encapsulation of Chemical Messengers for Intercellular Communication.
Journal of the American Chemical Society, 145(21):11499-11503.
In multicellular organisms, cells typically communicate by sending and receiving chemical signals. Chemical messengers involved in the exocytosis of neuroendocrine cells or neurons are generally assumed to only originate from the fusing of intracellular large dense core vesicles (LDCVs) or synaptic vesicles with the cellular membrane following stimulation. Accumulated evidence suggests that exosomes─one of the main extracellular vesicles (EVs)─carrying cell-dependent DNA, mRNA, proteins, etc., play an essential role in cellular communication. Due to experimental limitations, it has been difficult to monitor the real-time release of individual exosomes; this restricts a comprehensive understanding of the basic molecular mechanisms and the functions of exosomes. In this work, we introduce amperometry with microelectrodes to capture the dynamic release of single exosomes from a single living cell, distinguish them from other EVs, and differentiate the molecules inside exosomes and those secreted from LDCVs. We show that, similar to many LDCVs and synaptic vesicles, exosomes released by neuroendocrine cells also contain catecholamine transmitters. This finding reveals a different mode of chemical communication via exosome-encapsulated chemical messengers and a potential interconnection between the two release pathways, changing the canonical view of exocytosis of neuroendocrine cells and possibly neurons. This defines a new mechanism for chemical communication at the fundamental level and opens new avenues in the research of the molecular biology of exosomes in the neuroendocrine and central nervous systems.
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@article {pmid37205856,
year = {2023},
author = {Hu, K and Le Vo, KL and Wang, F and Zhang, X and Gu, C and Fang, N and Phan, NTN and Ewing, AG},
title = {Single Exosome Amperometric Measurements Reveal Encapsulation of Chemical Messengers for Intercellular Communication.},
journal = {Journal of the American Chemical Society},
volume = {145},
number = {21},
pages = {11499-11503},
doi = {10.1021/jacs.3c02844},
pmid = {37205856},
issn = {1520-5126},
mesh = {*Exosomes/metabolism ; *Extracellular Vesicles/metabolism ; Cell Communication ; Cell Membrane/metabolism ; Neurons ; },
abstract = {In multicellular organisms, cells typically communicate by sending and receiving chemical signals. Chemical messengers involved in the exocytosis of neuroendocrine cells or neurons are generally assumed to only originate from the fusing of intracellular large dense core vesicles (LDCVs) or synaptic vesicles with the cellular membrane following stimulation. Accumulated evidence suggests that exosomes─one of the main extracellular vesicles (EVs)─carrying cell-dependent DNA, mRNA, proteins, etc., play an essential role in cellular communication. Due to experimental limitations, it has been difficult to monitor the real-time release of individual exosomes; this restricts a comprehensive understanding of the basic molecular mechanisms and the functions of exosomes. In this work, we introduce amperometry with microelectrodes to capture the dynamic release of single exosomes from a single living cell, distinguish them from other EVs, and differentiate the molecules inside exosomes and those secreted from LDCVs. We show that, similar to many LDCVs and synaptic vesicles, exosomes released by neuroendocrine cells also contain catecholamine transmitters. This finding reveals a different mode of chemical communication via exosome-encapsulated chemical messengers and a potential interconnection between the two release pathways, changing the canonical view of exocytosis of neuroendocrine cells and possibly neurons. This defines a new mechanism for chemical communication at the fundamental level and opens new avenues in the research of the molecular biology of exosomes in the neuroendocrine and central nervous systems.},
}
MeSH Terms:
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*Exosomes/metabolism
*Extracellular Vesicles/metabolism
Cell Communication
Cell Membrane/metabolism
Neurons
RevDate: 2023-05-18
Evolution and phylogenetic distribution of endo-α-mannosidase.
Glycobiology pii:7171919 [Epub ahead of print].
While glycans underlie many biological processes, such as protein folding, cell adhesion and cell-cell recognition, deep evolution of glycosylation machinery remains an understudied topic. N-linked glycosylation is a conserved process in which mannosidases are key trimming enzymes. One of them is the glycoprotein endo-α-1,2-mannosidase which participates in the initial trimming of mannose moieties from an N-linked glycan inside the cis-Golgi. It is unique as the only endo-acting mannosidase found in this organelle. Relatively little is known about its origins and evolutionary history; so far it was reported to occur only in vertebrates. In this work, a taxon-rich bioinformatic survey to unravel the evolutionary history of this enzyme, including all major eukaryotic clades and a wide representation of animals, is presented. The endomannosidase was found to be more widely distributed in animals and other eukaryotes. The protein motif changes in context of the canonical animal enzyme were tracked. Additionally, the data show the two canonical vertebrate endomannosidase genes, MANEA and MANEAL, arose at the second round of the two vertebrate genome duplications and one more vertebrate paralog, CMANEAL, is uncovered. Finally, a framework where N-glycosylation co-evolved with complex multicellularity is described. A better understanding of the evolution of core glycosylation pathways is pivotal to understanding biology of eukaryotes in general, and the Golgi apparatus in particular. This systematic analysis of the endomannosidase evolution is one step towards this goal.
Additional Links: PMID-37202179
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@article {pmid37202179,
year = {2023},
author = {Sobala, ŁF},
title = {Evolution and phylogenetic distribution of endo-α-mannosidase.},
journal = {Glycobiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/glycob/cwad041},
pmid = {37202179},
issn = {1460-2423},
abstract = {While glycans underlie many biological processes, such as protein folding, cell adhesion and cell-cell recognition, deep evolution of glycosylation machinery remains an understudied topic. N-linked glycosylation is a conserved process in which mannosidases are key trimming enzymes. One of them is the glycoprotein endo-α-1,2-mannosidase which participates in the initial trimming of mannose moieties from an N-linked glycan inside the cis-Golgi. It is unique as the only endo-acting mannosidase found in this organelle. Relatively little is known about its origins and evolutionary history; so far it was reported to occur only in vertebrates. In this work, a taxon-rich bioinformatic survey to unravel the evolutionary history of this enzyme, including all major eukaryotic clades and a wide representation of animals, is presented. The endomannosidase was found to be more widely distributed in animals and other eukaryotes. The protein motif changes in context of the canonical animal enzyme were tracked. Additionally, the data show the two canonical vertebrate endomannosidase genes, MANEA and MANEAL, arose at the second round of the two vertebrate genome duplications and one more vertebrate paralog, CMANEAL, is uncovered. Finally, a framework where N-glycosylation co-evolved with complex multicellularity is described. A better understanding of the evolution of core glycosylation pathways is pivotal to understanding biology of eukaryotes in general, and the Golgi apparatus in particular. This systematic analysis of the endomannosidase evolution is one step towards this goal.},
}
RevDate: 2023-06-05
CmpDate: 2023-06-05
Virus-Induced Lysis of Tumor and Other Pathogenic Unicellular Entities and Its Potential to Treat Leishmaniasis.
DNA and cell biology, 42(6):305-314.
This article is focused on the main pathways used by viruses to achieve infection and lysis of unicellular eukaryotes described as pathogenic for multicellular organisms. In light of the recent discussions on how tumor cells exhibit unicellular behavior, highly malignant cells can be considered as another unicellular pathogenic entity, but with endogenous origin. Thus, a comparative panel of viral lysis of exogenous pathogenic unicellular eukaryotes such as Acanthamoeba sp., yeast, and tumors is presented. The important intracellular parasite Leishmania sp is also presented, which, in contrast, has its virulence improved by viral infections. The possible exploitation of viral-mediated eukaryotic cell lysis to overcome infections of Leishmania sp is discussed.
Additional Links: PMID-37195672
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@article {pmid37195672,
year = {2023},
author = {Fernandes, J},
title = {Virus-Induced Lysis of Tumor and Other Pathogenic Unicellular Entities and Its Potential to Treat Leishmaniasis.},
journal = {DNA and cell biology},
volume = {42},
number = {6},
pages = {305-314},
doi = {10.1089/dna.2023.0048},
pmid = {37195672},
issn = {1557-7430},
mesh = {Humans ; *Leishmaniasis/drug therapy/parasitology ; *Leishmania/metabolism ; Cell Death ; *Neoplasms ; Saccharomyces cerevisiae ; *Viruses ; },
abstract = {This article is focused on the main pathways used by viruses to achieve infection and lysis of unicellular eukaryotes described as pathogenic for multicellular organisms. In light of the recent discussions on how tumor cells exhibit unicellular behavior, highly malignant cells can be considered as another unicellular pathogenic entity, but with endogenous origin. Thus, a comparative panel of viral lysis of exogenous pathogenic unicellular eukaryotes such as Acanthamoeba sp., yeast, and tumors is presented. The important intracellular parasite Leishmania sp is also presented, which, in contrast, has its virulence improved by viral infections. The possible exploitation of viral-mediated eukaryotic cell lysis to overcome infections of Leishmania sp is discussed.},
}
MeSH Terms:
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Humans
*Leishmaniasis/drug therapy/parasitology
*Leishmania/metabolism
Cell Death
*Neoplasms
Saccharomyces cerevisiae
*Viruses
RevDate: 2023-05-17
CmpDate: 2023-05-16
Cis-regulatory landscapes in the evolution and development of the mammalian skull.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 378(1880):20220079.
Extensive morphological variation found in mammals reflects the wide spectrum of their ecological adaptations. The highest morphological diversity is present in the craniofacial region, where geometry is mainly dictated by the bony skull. Mammalian craniofacial development represents complex multistep processes governed by numerous conserved genes that require precise spatio-temporal control. A central question in contemporary evolutionary biology is how a defined set of conserved genes can orchestrate formation of fundamentally different structures, and therefore how morphological variability arises. In principle, differential gene expression patterns during development are the source of morphological variation. With the emergence of multicellular organisms, precise regulation of gene expression in time and space is attributed to cis-regulatory elements. These elements contribute to higher-order chromatin structure and together with trans-acting factors control transcriptional landscapes that underlie intricate morphogenetic processes. Consequently, divergence in cis-regulation is believed to rewire existing gene regulatory networks and form the core of morphological evolution. This review outlines the fundamental principles of the genetic code and genomic regulation interplay during development. Recent work that deepened our comprehension of cis-regulatory element origin, divergence and function is presented here to illustrate the state-of-the-art research that uncovered the principles of morphological novelty. This article is part of the theme issue 'The mammalian skull: development, structure and function'.
Additional Links: PMID-37183897
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@article {pmid37183897,
year = {2023},
author = {Kaucka, M},
title = {Cis-regulatory landscapes in the evolution and development of the mammalian skull.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {378},
number = {1880},
pages = {20220079},
pmid = {37183897},
issn = {1471-2970},
mesh = {Animals ; *Evolution, Molecular ; *Mammals/genetics ; Gene Regulatory Networks ; Skull ; Head ; },
abstract = {Extensive morphological variation found in mammals reflects the wide spectrum of their ecological adaptations. The highest morphological diversity is present in the craniofacial region, where geometry is mainly dictated by the bony skull. Mammalian craniofacial development represents complex multistep processes governed by numerous conserved genes that require precise spatio-temporal control. A central question in contemporary evolutionary biology is how a defined set of conserved genes can orchestrate formation of fundamentally different structures, and therefore how morphological variability arises. In principle, differential gene expression patterns during development are the source of morphological variation. With the emergence of multicellular organisms, precise regulation of gene expression in time and space is attributed to cis-regulatory elements. These elements contribute to higher-order chromatin structure and together with trans-acting factors control transcriptional landscapes that underlie intricate morphogenetic processes. Consequently, divergence in cis-regulation is believed to rewire existing gene regulatory networks and form the core of morphological evolution. This review outlines the fundamental principles of the genetic code and genomic regulation interplay during development. Recent work that deepened our comprehension of cis-regulatory element origin, divergence and function is presented here to illustrate the state-of-the-art research that uncovered the principles of morphological novelty. This article is part of the theme issue 'The mammalian skull: development, structure and function'.},
}
MeSH Terms:
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Animals
*Evolution, Molecular
*Mammals/genetics
Gene Regulatory Networks
Skull
Head
RevDate: 2023-05-15
CmpDate: 2023-05-15
Palmelloid Formation and Cell Aggregation Are Essential Mechanisms for High Light Tolerance in a Natural Strain of Chlamydomonas reinhardtii.
International journal of molecular sciences, 24(9):.
Photosynthetic organisms, such as higher plants and algae, require light to survive. However, an excessive amount of light can be harmful due to the production of reactive oxygen species (ROS), which cause cell damage and, if it is not effectively regulated, cell death. The study of plants' responses to light can aid in the development of methods to improve plants' growth and productivity. Due to the multicellular nature of plants, there may be variations in the results based on plant age and tissue type. Chlamydomonas reinhardtii, a unicellular green alga, has also been used as a model organism to study photosynthesis and photoprotection. Nonetheless, the majority of the research has been conducted with strains that have been consistently utilized in laboratories and originated from the same source. Despite the availability of many field isolates of this species, very few studies have compared the light responses of field isolates. This study examined the responses of two field isolates of Chlamydomonas to high light stress. The light-tolerant strain, CC-4414, managed reactive oxygen species (ROS) slightly better than the sensitive strain, CC-2344, did. The proteomic data of cells subjected to high light revealed cellular modifications of the light-tolerant strain toward membrane proteins. The morphology of cells under light stress revealed that this strain utilized the formation of palmelloid structures and cell aggregation to shield cells from excessive light. As indicated by proteome data, morphological modifications occur simultaneously with the increase in protein degradation and autophagy. By protecting cells from stress, cells are able to continue to upregulate ROS management mechanisms and prevent cell death. This is the first report of palmelloid formation in Chlamydomonas under high light stress.
Additional Links: PMID-37176080
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@article {pmid37176080,
year = {2023},
author = {Suwannachuen, N and Leetanasaksakul, K and Roytrakul, S and Phaonakrop, N and Thaisakun, S and Roongsattham, P and Jantasuriyarat, C and Sanevas, N and Sirikhachornkit, A},
title = {Palmelloid Formation and Cell Aggregation Are Essential Mechanisms for High Light Tolerance in a Natural Strain of Chlamydomonas reinhardtii.},
journal = {International journal of molecular sciences},
volume = {24},
number = {9},
pages = {},
pmid = {37176080},
issn = {1422-0067},
support = {This project is funded by National Research Council of Thailand (NRCT) and Kasetsart Univer-sity : N42A650287. This research and innovation activity is funded by National Research Council of Thailand (NRCT). This research is supported in part by the Grad//This project is funded by National Research Council of Thailand (NRCT) and Kasetsart Univer-sity : N42A650287. This research and innovation activity is funded by National Research Council of Thailand (NRCT). This research is supported in part by the Grad/ ; },
mesh = {*Chlamydomonas reinhardtii/metabolism ; Reactive Oxygen Species/metabolism ; Proteomics ; *Chlamydomonas/metabolism ; Photosynthesis/physiology ; },
abstract = {Photosynthetic organisms, such as higher plants and algae, require light to survive. However, an excessive amount of light can be harmful due to the production of reactive oxygen species (ROS), which cause cell damage and, if it is not effectively regulated, cell death. The study of plants' responses to light can aid in the development of methods to improve plants' growth and productivity. Due to the multicellular nature of plants, there may be variations in the results based on plant age and tissue type. Chlamydomonas reinhardtii, a unicellular green alga, has also been used as a model organism to study photosynthesis and photoprotection. Nonetheless, the majority of the research has been conducted with strains that have been consistently utilized in laboratories and originated from the same source. Despite the availability of many field isolates of this species, very few studies have compared the light responses of field isolates. This study examined the responses of two field isolates of Chlamydomonas to high light stress. The light-tolerant strain, CC-4414, managed reactive oxygen species (ROS) slightly better than the sensitive strain, CC-2344, did. The proteomic data of cells subjected to high light revealed cellular modifications of the light-tolerant strain toward membrane proteins. The morphology of cells under light stress revealed that this strain utilized the formation of palmelloid structures and cell aggregation to shield cells from excessive light. As indicated by proteome data, morphological modifications occur simultaneously with the increase in protein degradation and autophagy. By protecting cells from stress, cells are able to continue to upregulate ROS management mechanisms and prevent cell death. This is the first report of palmelloid formation in Chlamydomonas under high light stress.},
}
MeSH Terms:
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*Chlamydomonas reinhardtii/metabolism
Reactive Oxygen Species/metabolism
Proteomics
*Chlamydomonas/metabolism
Photosynthesis/physiology
RevDate: 2023-05-15
CmpDate: 2023-05-15
The influence of immune challenges on the mean and variance in reproductive investment: a meta-analysis of the terminal investment hypothesis.
BMC biology, 21(1):107.
Finding the optimal balance between survival and reproduction is a central puzzle in life-history theory. The terminal investment hypothesis predicts that when individuals encounter a survival threat that compromises future reproductive potential, they will increase immediate reproductive investment to maximise fitness. Despite decades of research on the terminal investment hypothesis, findings remain mixed. We examined the terminal investment hypothesis with a meta-analysis of studies that measured reproductive investment of multicellular iteroparous animals after a non-lethal immune challenge. We had two main aims. The first was to investigate whether individuals, on average, increase reproductive investment in response to an immune threat, as predicted by the terminal investment hypothesis. We also examined whether such responses vary adaptively on factors associated with the amount of reproductive opportunities left (residual reproductive value) in the individuals, as predicted by the terminal investment hypothesis. The second was to provide a quantitative test of a novel prediction based on the dynamic threshold model: that an immune threat increases between-individual variance in reproductive investment. Our results provided some support for our hypotheses. Older individuals, who are expected to have lower residual reproductive values, showed stronger mean terminal investment response than younger individuals. In terms of variance, individuals showed a divergence in responses, leading to an increase in variance. This increase in variance was especially amplified in longer-living species, which was consistent with our prediction that individuals in longer-living species should respond with greater individual variation due to increased phenotypic plasticity. We find little statistical evidence of publication bias. Together, our results highlight the need for a more nuanced view on the terminal investment hypothesis and a greater focus on the factors that drive individual responses.
Additional Links: PMID-37173684
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Citation:
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@article {pmid37173684,
year = {2023},
author = {Foo, YZ and Lagisz, M and O'Dea, RE and Nakagawa, S},
title = {The influence of immune challenges on the mean and variance in reproductive investment: a meta-analysis of the terminal investment hypothesis.},
journal = {BMC biology},
volume = {21},
number = {1},
pages = {107},
pmid = {37173684},
issn = {1741-7007},
mesh = {Animals ; *Reproduction/physiology ; },
abstract = {Finding the optimal balance between survival and reproduction is a central puzzle in life-history theory. The terminal investment hypothesis predicts that when individuals encounter a survival threat that compromises future reproductive potential, they will increase immediate reproductive investment to maximise fitness. Despite decades of research on the terminal investment hypothesis, findings remain mixed. We examined the terminal investment hypothesis with a meta-analysis of studies that measured reproductive investment of multicellular iteroparous animals after a non-lethal immune challenge. We had two main aims. The first was to investigate whether individuals, on average, increase reproductive investment in response to an immune threat, as predicted by the terminal investment hypothesis. We also examined whether such responses vary adaptively on factors associated with the amount of reproductive opportunities left (residual reproductive value) in the individuals, as predicted by the terminal investment hypothesis. The second was to provide a quantitative test of a novel prediction based on the dynamic threshold model: that an immune threat increases between-individual variance in reproductive investment. Our results provided some support for our hypotheses. Older individuals, who are expected to have lower residual reproductive values, showed stronger mean terminal investment response than younger individuals. In terms of variance, individuals showed a divergence in responses, leading to an increase in variance. This increase in variance was especially amplified in longer-living species, which was consistent with our prediction that individuals in longer-living species should respond with greater individual variation due to increased phenotypic plasticity. We find little statistical evidence of publication bias. Together, our results highlight the need for a more nuanced view on the terminal investment hypothesis and a greater focus on the factors that drive individual responses.},
}
MeSH Terms:
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Animals
*Reproduction/physiology
RevDate: 2023-06-01
CmpDate: 2023-06-01
De novo evolution of macroscopic multicellularity.
Nature, 617(7962):747-754.
While early multicellular lineages necessarily started out as relatively simple groups of cells, little is known about how they became Darwinian entities capable of sustained multicellular evolution[1-3]. Here we investigate this with a multicellularity long-term evolution experiment, selecting for larger group size in the snowflake yeast (Saccharomyces cerevisiae) model system. Given the historical importance of oxygen limitation[4], our ongoing experiment consists of three metabolic treatments[5]-anaerobic, obligately aerobic and mixotrophic yeast. After 600 rounds of selection, snowflake yeast in the anaerobic treatment group evolved to be macroscopic, becoming around 2 × 10[4] times larger (approximately mm scale) and about 10[4]-fold more biophysically tough, while retaining a clonal multicellular life cycle. This occurred through biophysical adaptation-evolution of increasingly elongate cells that initially reduced the strain of cellular packing and then facilitated branch entanglements that enabled groups of cells to stay together even after many cellular bonds fracture. By contrast, snowflake yeast competing for low oxygen[5] remained microscopic, evolving to be only around sixfold larger, underscoring the critical role of oxygen levels in the evolution of multicellular size. Together, this research provides unique insights into an ongoing evolutionary transition in individuality, showing how simple groups of cells overcome fundamental biophysical limitations through gradual, yet sustained, multicellular evolution.
Additional Links: PMID-37165189
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Citation:
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@article {pmid37165189,
year = {2023},
author = {Bozdag, GO and Zamani-Dahaj, SA and Day, TC and Kahn, PC and Burnetti, AJ and Lac, DT and Tong, K and Conlin, PL and Balwani, AH and Dyer, EL and Yunker, PJ and Ratcliff, WC},
title = {De novo evolution of macroscopic multicellularity.},
journal = {Nature},
volume = {617},
number = {7962},
pages = {747-754},
pmid = {37165189},
issn = {1476-4687},
support = {R35 GM138354/GM/NIGMS NIH HHS/United States ; },
mesh = {*Acclimatization ; *Biological Evolution ; Models, Biological ; *Saccharomyces cerevisiae/cytology/metabolism ; Anaerobiosis ; Aerobiosis ; Oxygen/analysis/metabolism ; Cell Shape ; *Cell Aggregation/physiology ; },
abstract = {While early multicellular lineages necessarily started out as relatively simple groups of cells, little is known about how they became Darwinian entities capable of sustained multicellular evolution[1-3]. Here we investigate this with a multicellularity long-term evolution experiment, selecting for larger group size in the snowflake yeast (Saccharomyces cerevisiae) model system. Given the historical importance of oxygen limitation[4], our ongoing experiment consists of three metabolic treatments[5]-anaerobic, obligately aerobic and mixotrophic yeast. After 600 rounds of selection, snowflake yeast in the anaerobic treatment group evolved to be macroscopic, becoming around 2 × 10[4] times larger (approximately mm scale) and about 10[4]-fold more biophysically tough, while retaining a clonal multicellular life cycle. This occurred through biophysical adaptation-evolution of increasingly elongate cells that initially reduced the strain of cellular packing and then facilitated branch entanglements that enabled groups of cells to stay together even after many cellular bonds fracture. By contrast, snowflake yeast competing for low oxygen[5] remained microscopic, evolving to be only around sixfold larger, underscoring the critical role of oxygen levels in the evolution of multicellular size. Together, this research provides unique insights into an ongoing evolutionary transition in individuality, showing how simple groups of cells overcome fundamental biophysical limitations through gradual, yet sustained, multicellular evolution.},
}
MeSH Terms:
show MeSH Terms
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*Acclimatization
*Biological Evolution
Models, Biological
*Saccharomyces cerevisiae/cytology/metabolism
Anaerobiosis
Aerobiosis
Oxygen/analysis/metabolism
Cell Shape
*Cell Aggregation/physiology
RevDate: 2023-05-13
CmpDate: 2023-05-11
Evolution: Understanding the origins of facultative multicellular life cycles.
Current biology : CB, 33(9):R356-R358.
Multicellular organisms exhibit a fascinating diversity of life cycles, but little is known about the factors governing life-cycle evolution. New studies of wild yeast and cyanobacteria provide insight into how and why facultative multicellular life cycles arise.
Additional Links: PMID-37160092
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@article {pmid37160092,
year = {2023},
author = {Conlin, PL and Ratcliff, WC},
title = {Evolution: Understanding the origins of facultative multicellular life cycles.},
journal = {Current biology : CB},
volume = {33},
number = {9},
pages = {R356-R358},
doi = {10.1016/j.cub.2023.03.065},
pmid = {37160092},
issn = {1879-0445},
mesh = {Animals ; *Life Cycle Stages ; *Saccharomyces cerevisiae ; },
abstract = {Multicellular organisms exhibit a fascinating diversity of life cycles, but little is known about the factors governing life-cycle evolution. New studies of wild yeast and cyanobacteria provide insight into how and why facultative multicellular life cycles arise.},
}
MeSH Terms:
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Animals
*Life Cycle Stages
*Saccharomyces cerevisiae
RevDate: 2023-05-09
Reuniting philosophy and science to advance cancer research.
Biological reviews of the Cambridge Philosophical Society [Epub ahead of print].
Cancers rely on multiple, heterogeneous processes at different scales, pertaining to many biomedical fields. Therefore, understanding cancer is necessarily an interdisciplinary task that requires placing specialised experimental and clinical research into a broader conceptual, theoretical, and methodological framework. Without such a framework, oncology will collect piecemeal results, with scant dialogue between the different scientific communities studying cancer. We argue that one important way forward in service of a more successful dialogue is through greater integration of applied sciences (experimental and clinical) with conceptual and theoretical approaches, informed by philosophical methods. By way of illustration, we explore six central themes: (i) the role of mutations in cancer; (ii) the clonal evolution of cancer cells; (iii) the relationship between cancer and multicellularity; (iv) the tumour microenvironment; (v) the immune system; and (vi) stem cells. In each case, we examine open questions in the scientific literature through a philosophical methodology and show the benefit of such a synergy for the scientific and medical understanding of cancer.
Additional Links: PMID-37157910
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@article {pmid37157910,
year = {2023},
author = {Pradeu, T and Daignan-Fornier, B and Ewald, A and Germain, PL and Okasha, S and Plutynski, A and Benzekry, S and Bertolaso, M and Bissell, M and Brown, JS and Chin-Yee, B and Chin-Yee, I and Clevers, H and Cognet, L and Darrason, M and Farge, E and Feunteun, J and Galon, J and Giroux, E and Green, S and Gross, F and Jaulin, F and Knight, R and Laconi, E and Larmonier, N and Maley, C and Mantovani, A and Moreau, V and Nassoy, P and Rondeau, E and Santamaria, D and Sawai, CM and Seluanov, A and Sepich-Poore, GD and Sisirak, V and Solary, E and Yvonnet, S and Laplane, L},
title = {Reuniting philosophy and science to advance cancer research.},
journal = {Biological reviews of the Cambridge Philosophical Society},
volume = {},
number = {},
pages = {},
doi = {10.1111/brv.12971},
pmid = {37157910},
issn = {1469-185X},
support = {ANR-19-CE27-0027-01//Agence Nationale de la Recherche/ ; //SIRIC-Brio/ ; //Région Nouvelle Aquitaine/ ; GBMF9021//Gordon and Betty Moore Foundation/ ; 2021-1-EMERG-54-CNRS DR 5-1//Canceropôle Emergence/ ; //CNRS program/ ; EL2020//Ligue National Contre le Cancer Equipe labelisée/ ; },
abstract = {Cancers rely on multiple, heterogeneous processes at different scales, pertaining to many biomedical fields. Therefore, understanding cancer is necessarily an interdisciplinary task that requires placing specialised experimental and clinical research into a broader conceptual, theoretical, and methodological framework. Without such a framework, oncology will collect piecemeal results, with scant dialogue between the different scientific communities studying cancer. We argue that one important way forward in service of a more successful dialogue is through greater integration of applied sciences (experimental and clinical) with conceptual and theoretical approaches, informed by philosophical methods. By way of illustration, we explore six central themes: (i) the role of mutations in cancer; (ii) the clonal evolution of cancer cells; (iii) the relationship between cancer and multicellularity; (iv) the tumour microenvironment; (v) the immune system; and (vi) stem cells. In each case, we examine open questions in the scientific literature through a philosophical methodology and show the benefit of such a synergy for the scientific and medical understanding of cancer.},
}
RevDate: 2023-06-19
CmpDate: 2023-05-10
Darwin's agential materials: evolutionary implications of multiscale competency in developmental biology.
Cellular and molecular life sciences : CMLS, 80(6):142.
A critical aspect of evolution is the layer of developmental physiology that operates between the genotype and the anatomical phenotype. While much work has addressed the evolution of developmental mechanisms and the evolvability of specific genetic architectures with emergent complexity, one aspect has not been sufficiently explored: the implications of morphogenetic problem-solving competencies for the evolutionary process itself. The cells that evolution works with are not passive components: rather, they have numerous capabilities for behavior because they derive from ancestral unicellular organisms with rich repertoires. In multicellular organisms, these capabilities must be tamed, and can be exploited, by the evolutionary process. Specifically, biological structures have a multiscale competency architecture where cells, tissues, and organs exhibit regulative plasticity-the ability to adjust to perturbations such as external injury or internal modifications and still accomplish specific adaptive tasks across metabolic, transcriptional, physiological, and anatomical problem spaces. Here, I review examples illustrating how physiological circuits guiding cellular collective behavior impart computational properties to the agential material that serves as substrate for the evolutionary process. I then explore the ways in which the collective intelligence of cells during morphogenesis affect evolution, providing a new perspective on the evolutionary search process. This key feature of the physiological software of life helps explain the remarkable speed and robustness of biological evolution, and sheds new light on the relationship between genomes and functional anatomical phenotypes.
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@article {pmid37156924,
year = {2023},
author = {Levin, M},
title = {Darwin's agential materials: evolutionary implications of multiscale competency in developmental biology.},
journal = {Cellular and molecular life sciences : CMLS},
volume = {80},
number = {6},
pages = {142},
pmid = {37156924},
issn = {1420-9071},
support = {62212//John Templeton Foundation/ ; },
mesh = {*Biological Evolution ; Genotype ; *Genome ; Phenotype ; Developmental Biology ; },
abstract = {A critical aspect of evolution is the layer of developmental physiology that operates between the genotype and the anatomical phenotype. While much work has addressed the evolution of developmental mechanisms and the evolvability of specific genetic architectures with emergent complexity, one aspect has not been sufficiently explored: the implications of morphogenetic problem-solving competencies for the evolutionary process itself. The cells that evolution works with are not passive components: rather, they have numerous capabilities for behavior because they derive from ancestral unicellular organisms with rich repertoires. In multicellular organisms, these capabilities must be tamed, and can be exploited, by the evolutionary process. Specifically, biological structures have a multiscale competency architecture where cells, tissues, and organs exhibit regulative plasticity-the ability to adjust to perturbations such as external injury or internal modifications and still accomplish specific adaptive tasks across metabolic, transcriptional, physiological, and anatomical problem spaces. Here, I review examples illustrating how physiological circuits guiding cellular collective behavior impart computational properties to the agential material that serves as substrate for the evolutionary process. I then explore the ways in which the collective intelligence of cells during morphogenesis affect evolution, providing a new perspective on the evolutionary search process. This key feature of the physiological software of life helps explain the remarkable speed and robustness of biological evolution, and sheds new light on the relationship between genomes and functional anatomical phenotypes.},
}
MeSH Terms:
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hide MeSH Terms
*Biological Evolution
Genotype
*Genome
Phenotype
Developmental Biology
RevDate: 2023-05-20
CmpDate: 2023-05-10
Evolutionary dynamics within and among competing groups.
Proceedings of the National Academy of Sciences of the United States of America, 120(20):e2216186120.
Biological and social systems are structured at multiple scales, and the incentives of individuals who interact in a group may diverge from the collective incentive of the group as a whole. Mechanisms to resolve this tension are responsible for profound transitions in evolutionary history, including the origin of cellular life, multicellular life, and even societies. Here, we synthesize a growing literature that extends evolutionary game theory to describe multilevel evolutionary dynamics, using nested birth-death processes and partial differential equations to model natural selection acting on competition within and among groups of individuals. We analyze how mechanisms known to promote cooperation within a single group-including assortment, reciprocity, and population structure-alter evolutionary outcomes in the presence of competition among groups. We find that population structures most conducive to cooperation in multiscale systems can differ from those most conducive within a single group. Likewise, for competitive interactions with a continuous range of strategies we find that among-group selection may fail to produce socially optimal outcomes, but it can nonetheless produce second-best solutions that balance individual incentives to defect with the collective incentives for cooperation. We conclude by describing the broad applicability of multiscale evolutionary models to problems ranging from the production of diffusible metabolites in microbes to the management of common-pool resources in human societies.
Additional Links: PMID-37155901
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@article {pmid37155901,
year = {2023},
author = {Cooney, DB and Levin, SA and Mori, Y and Plotkin, JB},
title = {Evolutionary dynamics within and among competing groups.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {120},
number = {20},
pages = {e2216186120},
pmid = {37155901},
issn = {1091-6490},
mesh = {Humans ; *Cooperative Behavior ; *Biological Evolution ; Selection, Genetic ; Game Theory ; },
abstract = {Biological and social systems are structured at multiple scales, and the incentives of individuals who interact in a group may diverge from the collective incentive of the group as a whole. Mechanisms to resolve this tension are responsible for profound transitions in evolutionary history, including the origin of cellular life, multicellular life, and even societies. Here, we synthesize a growing literature that extends evolutionary game theory to describe multilevel evolutionary dynamics, using nested birth-death processes and partial differential equations to model natural selection acting on competition within and among groups of individuals. We analyze how mechanisms known to promote cooperation within a single group-including assortment, reciprocity, and population structure-alter evolutionary outcomes in the presence of competition among groups. We find that population structures most conducive to cooperation in multiscale systems can differ from those most conducive within a single group. Likewise, for competitive interactions with a continuous range of strategies we find that among-group selection may fail to produce socially optimal outcomes, but it can nonetheless produce second-best solutions that balance individual incentives to defect with the collective incentives for cooperation. We conclude by describing the broad applicability of multiscale evolutionary models to problems ranging from the production of diffusible metabolites in microbes to the management of common-pool resources in human societies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Cooperative Behavior
*Biological Evolution
Selection, Genetic
Game Theory
RevDate: 2023-05-09
Cellular and Natural Viral Engineering in Cognition-Based Evolution.
Communicative & integrative biology, 16(1):2196145.
Neo-Darwinism conceptualizes evolution as the continuous succession of predominately random genetic variations disciplined by natural selection. In that frame, the primary interaction between cells and the virome is relegated to host-parasite dynamics governed by selective influences. Cognition-Based Evolution regards biological and evolutionary development as a reciprocating cognition-based informational interactome for the protection of self-referential cells. To sustain cellular homeorhesis, cognitive cells collaborate to assess the validity of ambiguous biological information. That collective interaction involves coordinate measurement, communication, and active deployment of resources as Natural Cellular Engineering. These coordinated activities drive multicellularity, biological development, and evolutionary change. The virome participates as the vital intercessory among the cellular domains to ensure their shared permanent perpetuation. The interactions between the virome and the cellular domains represent active virocellular cross-communications for the continual exchange of resources. Modular genetic transfers between viruses and cells carry bioactive potentials. Those exchanges are deployed as nonrandom flexible tools among the domains in their continuous confrontation with environmental stresses. This alternative framework fundamentally shifts our perspective on viral-cellular interactions, strengthening established principles of viral symbiogenesis. Pathogenesis can now be properly appraised as one expression of a range of outcomes between cells and viruses within a larger conceptual framework of Natural Viral Engineering as a co-engineering participant with cells. It is proposed that Natural Viral Engineering should be viewed as a co-existent facet of Natural Cellular Engineering within Cognition-Based Evolution.
Additional Links: PMID-37153718
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@article {pmid37153718,
year = {2023},
author = {W B, M and A S, R and P, M and F, B},
title = {Cellular and Natural Viral Engineering in Cognition-Based Evolution.},
journal = {Communicative & integrative biology},
volume = {16},
number = {1},
pages = {2196145},
pmid = {37153718},
issn = {1942-0889},
abstract = {Neo-Darwinism conceptualizes evolution as the continuous succession of predominately random genetic variations disciplined by natural selection. In that frame, the primary interaction between cells and the virome is relegated to host-parasite dynamics governed by selective influences. Cognition-Based Evolution regards biological and evolutionary development as a reciprocating cognition-based informational interactome for the protection of self-referential cells. To sustain cellular homeorhesis, cognitive cells collaborate to assess the validity of ambiguous biological information. That collective interaction involves coordinate measurement, communication, and active deployment of resources as Natural Cellular Engineering. These coordinated activities drive multicellularity, biological development, and evolutionary change. The virome participates as the vital intercessory among the cellular domains to ensure their shared permanent perpetuation. The interactions between the virome and the cellular domains represent active virocellular cross-communications for the continual exchange of resources. Modular genetic transfers between viruses and cells carry bioactive potentials. Those exchanges are deployed as nonrandom flexible tools among the domains in their continuous confrontation with environmental stresses. This alternative framework fundamentally shifts our perspective on viral-cellular interactions, strengthening established principles of viral symbiogenesis. Pathogenesis can now be properly appraised as one expression of a range of outcomes between cells and viruses within a larger conceptual framework of Natural Viral Engineering as a co-engineering participant with cells. It is proposed that Natural Viral Engineering should be viewed as a co-existent facet of Natural Cellular Engineering within Cognition-Based Evolution.},
}
RevDate: 2023-05-04
Spatiotemporal control of root immune responses during microbial colonization.
Current opinion in plant biology, 74:102369 pii:S1369-5266(23)00034-1 [Epub ahead of print].
The entire evolutionary trajectory of plants towards large and complex multi-cellular organisms has been accompanied by incessant interactions with omnipresent unicellular microbes. This led to the evolution of highly complex microbial communities, whose members display the entire spectrum of pathogenic to mutualistic behaviors. Plant roots are dynamic, fractally growing organs and even small Arabidopsis roots harbor millions of individual microbes of diverse taxa. It is evident that microbes at different positions on a root surface could experience fundamentally different environments, which, moreover, rapidly change over time. Differences in spatial scales between microbes and roots compares to humans and the cities they inhabit. Such considerations make it evident that mechanisms of root-microbe interactions can only be understood if analyzed at relevant spatial and temporal scales. This review attempts to provide an overview of the rapid recent progress that has been made in mapping and manipulating plant damage and immune responses at cellular resolution, as well as in visualizing bacterial communities and their transcriptional activities. We further discuss the impact that such approaches will have for a more predictive understanding of root-microbe interactions.
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@article {pmid37141807,
year = {2023},
author = {Tsai, HH and Wang, J and Geldner, N and Zhou, F},
title = {Spatiotemporal control of root immune responses during microbial colonization.},
journal = {Current opinion in plant biology},
volume = {74},
number = {},
pages = {102369},
doi = {10.1016/j.pbi.2023.102369},
pmid = {37141807},
issn = {1879-0356},
abstract = {The entire evolutionary trajectory of plants towards large and complex multi-cellular organisms has been accompanied by incessant interactions with omnipresent unicellular microbes. This led to the evolution of highly complex microbial communities, whose members display the entire spectrum of pathogenic to mutualistic behaviors. Plant roots are dynamic, fractally growing organs and even small Arabidopsis roots harbor millions of individual microbes of diverse taxa. It is evident that microbes at different positions on a root surface could experience fundamentally different environments, which, moreover, rapidly change over time. Differences in spatial scales between microbes and roots compares to humans and the cities they inhabit. Such considerations make it evident that mechanisms of root-microbe interactions can only be understood if analyzed at relevant spatial and temporal scales. This review attempts to provide an overview of the rapid recent progress that has been made in mapping and manipulating plant damage and immune responses at cellular resolution, as well as in visualizing bacterial communities and their transcriptional activities. We further discuss the impact that such approaches will have for a more predictive understanding of root-microbe interactions.},
}
RevDate: 2023-06-12
CmpDate: 2023-06-12
Low Spontaneous Mutation Rate in Complex Multicellular Eukaryotes with a Haploid-Diploid Life Cycle.
Molecular biology and evolution, 40(6):.
The spontaneous mutation rate µ is a crucial parameter to understand evolution and biodiversity. Mutation rates are highly variable across species, suggesting that µ is susceptible to selection and drift and that species life cycle and life history may impact its evolution. In particular, asexual reproduction and haploid selection are expected to affect the mutation rate, but very little empirical data are available to test this expectation. Here, we sequence 30 genomes of a parent-offspring pedigree in the model brown alga Ectocarpus sp.7, and 137 genomes of an interspecific cross of the closely related brown alga Scytosiphon to have access to the spontaneous mutation rate of representative organisms of a complex multicellular eukaryotic lineage outside animals and plants, and to evaluate the potential impact of life cycle on the mutation rate. Brown algae alternate between a haploid and a diploid stage, both multicellular and free living, and utilize both sexual and asexual reproduction. They are, therefore, excellent models to empirically test expectations of the effect of asexual reproduction and haploid selection on mutation rate evolution. We estimate that Ectocarpus has a base substitution rate of µbs = 4.07 × 10-10 per site per generation, whereas the Scytosiphon interspecific cross had µbs = 1.22 × 10-9. Overall, our estimations suggest that these brown algae, despite being multicellular complex eukaryotes, have unusually low mutation rates. In Ectocarpus, effective population size (Ne) could not entirely explain the low µbs. We propose that the haploid-diploid life cycle, combined with extensive asexual reproduction, may be additional key drivers of the mutation rate in these organisms.
Additional Links: PMID-37140022
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@article {pmid37140022,
year = {2023},
author = {Krasovec, M and Hoshino, M and Zheng, M and Lipinska, AP and Coelho, SM},
title = {Low Spontaneous Mutation Rate in Complex Multicellular Eukaryotes with a Haploid-Diploid Life Cycle.},
journal = {Molecular biology and evolution},
volume = {40},
number = {6},
pages = {},
pmid = {37140022},
issn = {1537-1719},
mesh = {Animals ; Haploidy ; *Diploidy ; Mutation Rate ; Eukaryota ; Life Cycle Stages/genetics ; Plants ; *Phaeophyta/genetics ; },
abstract = {The spontaneous mutation rate µ is a crucial parameter to understand evolution and biodiversity. Mutation rates are highly variable across species, suggesting that µ is susceptible to selection and drift and that species life cycle and life history may impact its evolution. In particular, asexual reproduction and haploid selection are expected to affect the mutation rate, but very little empirical data are available to test this expectation. Here, we sequence 30 genomes of a parent-offspring pedigree in the model brown alga Ectocarpus sp.7, and 137 genomes of an interspecific cross of the closely related brown alga Scytosiphon to have access to the spontaneous mutation rate of representative organisms of a complex multicellular eukaryotic lineage outside animals and plants, and to evaluate the potential impact of life cycle on the mutation rate. Brown algae alternate between a haploid and a diploid stage, both multicellular and free living, and utilize both sexual and asexual reproduction. They are, therefore, excellent models to empirically test expectations of the effect of asexual reproduction and haploid selection on mutation rate evolution. We estimate that Ectocarpus has a base substitution rate of µbs = 4.07 × 10-10 per site per generation, whereas the Scytosiphon interspecific cross had µbs = 1.22 × 10-9. Overall, our estimations suggest that these brown algae, despite being multicellular complex eukaryotes, have unusually low mutation rates. In Ectocarpus, effective population size (Ne) could not entirely explain the low µbs. We propose that the haploid-diploid life cycle, combined with extensive asexual reproduction, may be additional key drivers of the mutation rate in these organisms.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Haploidy
*Diploidy
Mutation Rate
Eukaryota
Life Cycle Stages/genetics
Plants
*Phaeophyta/genetics
RevDate: 2023-05-02
Amino acids integrate behaviors in nerveless placozoans.
Frontiers in neuroscience, 17:1125624.
Placozoans are the simplest known free-living animals without recognized neurons and muscles but a complex behavioral repertoire. However, mechanisms and cellular bases of behavioral coordination are unknown. Here, using Trichoplax adhaerens as a model, we described 0.02-0.002 Hz oscillations in locomotory and feeding patterns as evidence of complex multicellular integration; and showed their dependence on the endogenous secretion of signal molecules. Evolutionary conserved low-molecular-weight transmitters (glutamate, aspartate, glycine, GABA, and ATP) acted as coordinators of distinct locomotory and feeding patterns. Specifically, L-glutamate induced and partially mimicked endogenous feeding cycles, whereas glycine and GABA suppressed feeding. ATP-modified feeding is complex, first causing feeding-like cycles and then suppressing feeding. Trichoplax locomotion was modulated by glycine, GABA, and, surprisingly, by animals' own mucus trails. Mucus triples locomotory speed compared to clean substrates. Glycine and GABA increased the frequency of turns. The effects of the amino acids are likely mediated by numerous receptors (R), including those from ionotropic GluRs, metabotropic GluRs, and GABA-BR families. Eighty-five of these receptors are encoded in the Trichoplax genome, more than in any other animal sequenced. Phylogenetic reconstructions illuminate massive lineage-specific expansions of amino acid receptors in Placozoa, Cnidaria, and Porifera and parallel evolution of nutritional sensing. Furthermore, we view the integration of feeding behaviors in nerveless animals by amino acids as ancestral exaptations that pave the way for co-options of glutamate, glycine, GABA, and ATP as classical neurotransmitters in eumetazoans.
Additional Links: PMID-37123368
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Citation:
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@article {pmid37123368,
year = {2023},
author = {Nikitin, MA and Romanova, DY and Borman, SI and Moroz, LL},
title = {Amino acids integrate behaviors in nerveless placozoans.},
journal = {Frontiers in neuroscience},
volume = {17},
number = {},
pages = {1125624},
pmid = {37123368},
issn = {1662-4548},
abstract = {Placozoans are the simplest known free-living animals without recognized neurons and muscles but a complex behavioral repertoire. However, mechanisms and cellular bases of behavioral coordination are unknown. Here, using Trichoplax adhaerens as a model, we described 0.02-0.002 Hz oscillations in locomotory and feeding patterns as evidence of complex multicellular integration; and showed their dependence on the endogenous secretion of signal molecules. Evolutionary conserved low-molecular-weight transmitters (glutamate, aspartate, glycine, GABA, and ATP) acted as coordinators of distinct locomotory and feeding patterns. Specifically, L-glutamate induced and partially mimicked endogenous feeding cycles, whereas glycine and GABA suppressed feeding. ATP-modified feeding is complex, first causing feeding-like cycles and then suppressing feeding. Trichoplax locomotion was modulated by glycine, GABA, and, surprisingly, by animals' own mucus trails. Mucus triples locomotory speed compared to clean substrates. Glycine and GABA increased the frequency of turns. The effects of the amino acids are likely mediated by numerous receptors (R), including those from ionotropic GluRs, metabotropic GluRs, and GABA-BR families. Eighty-five of these receptors are encoded in the Trichoplax genome, more than in any other animal sequenced. Phylogenetic reconstructions illuminate massive lineage-specific expansions of amino acid receptors in Placozoa, Cnidaria, and Porifera and parallel evolution of nutritional sensing. Furthermore, we view the integration of feeding behaviors in nerveless animals by amino acids as ancestral exaptations that pave the way for co-options of glutamate, glycine, GABA, and ATP as classical neurotransmitters in eumetazoans.},
}
RevDate: 2023-05-02
CmpDate: 2023-05-01
The Genetics of Fitness Reorganization during the Transition to Multicellularity: The Volvocine regA-like Family as a Model.
Genes, 14(4):.
The evolutionary transition from single-celled to multicellular individuality requires organismal fitness to shift from the cell level to a cell group. This reorganization of fitness occurs by re-allocating the two components of fitness, survival and reproduction, between two specialized cell types in the multicellular group: soma and germ, respectively. How does the genetic basis for such fitness reorganization evolve? One possible mechanism is the co-option of life history genes present in the unicellular ancestors of a multicellular lineage. For instance, single-celled organisms must regulate their investment in survival and reproduction in response to environmental changes, particularly decreasing reproduction to ensure survival under stress. Such stress response life history genes can provide the genetic basis for the evolution of cellular differentiation in multicellular lineages. The regA-like gene family in the volvocine green algal lineage provides an excellent model system to study how this co-option can occur. We discuss the origin and evolution of the volvocine regA-like gene family, including regA-the gene that controls somatic cell development in the model organism Volvox carteri. We hypothesize that the co-option of life history trade-off genes is a general mechanism involved in the transition to multicellular individuality, making volvocine algae and the regA-like family a useful template for similar investigations in other lineages.
Additional Links: PMID-37107699
PubMed:
Citation:
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@article {pmid37107699,
year = {2023},
author = {Grochau-Wright, ZI and Nedelcu, AM and Michod, RE},
title = {The Genetics of Fitness Reorganization during the Transition to Multicellularity: The Volvocine regA-like Family as a Model.},
journal = {Genes},
volume = {14},
number = {4},
pages = {},
pmid = {37107699},
issn = {2073-4425},
mesh = {Phylogeny ; *Chlorophyta ; *Volvox/genetics ; Models, Biological ; Cell Differentiation/genetics ; },
abstract = {The evolutionary transition from single-celled to multicellular individuality requires organismal fitness to shift from the cell level to a cell group. This reorganization of fitness occurs by re-allocating the two components of fitness, survival and reproduction, between two specialized cell types in the multicellular group: soma and germ, respectively. How does the genetic basis for such fitness reorganization evolve? One possible mechanism is the co-option of life history genes present in the unicellular ancestors of a multicellular lineage. For instance, single-celled organisms must regulate their investment in survival and reproduction in response to environmental changes, particularly decreasing reproduction to ensure survival under stress. Such stress response life history genes can provide the genetic basis for the evolution of cellular differentiation in multicellular lineages. The regA-like gene family in the volvocine green algal lineage provides an excellent model system to study how this co-option can occur. We discuss the origin and evolution of the volvocine regA-like gene family, including regA-the gene that controls somatic cell development in the model organism Volvox carteri. We hypothesize that the co-option of life history trade-off genes is a general mechanism involved in the transition to multicellular individuality, making volvocine algae and the regA-like family a useful template for similar investigations in other lineages.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Phylogeny
*Chlorophyta
*Volvox/genetics
Models, Biological
Cell Differentiation/genetics
RevDate: 2023-05-02
CmpDate: 2023-05-01
Computational Biology Helps Understand How Polyploid Giant Cancer Cells Drive Tumor Success.
Genes, 14(4):.
Precision and organization govern the cell cycle, ensuring normal proliferation. However, some cells may undergo abnormal cell divisions (neosis) or variations of mitotic cycles (endopolyploidy). Consequently, the formation of polyploid giant cancer cells (PGCCs), critical for tumor survival, resistance, and immortalization, can occur. Newly formed cells end up accessing numerous multicellular and unicellular programs that enable metastasis, drug resistance, tumor recurrence, and self-renewal or diverse clone formation. An integrative literature review was carried out, searching articles in several sites, including: PUBMED, NCBI-PMC, and Google Academic, published in English, indexed in referenced databases and without a publication time filter, but prioritizing articles from the last 3 years, to answer the following questions: (i) "What is the current knowledge about polyploidy in tumors?"; (ii) "What are the applications of computational studies for the understanding of cancer polyploidy?"; and (iii) "How do PGCCs contribute to tumorigenesis?"
Additional Links: PMID-37107559
PubMed:
Citation:
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@article {pmid37107559,
year = {2023},
author = {Casotti, MC and Meira, DD and Zetum, ASS and Araújo, BC and Silva, DRCD and Santos, EVWD and Garcia, FM and Paula, F and Santana, GM and Louro, LS and Alves, LNR and Braga, RFR and Trabach, RSDR and Bernardes, SS and Louro, TES and Chiela, ECF and Lenz, G and Carvalho, EF and Louro, ID},
title = {Computational Biology Helps Understand How Polyploid Giant Cancer Cells Drive Tumor Success.},
journal = {Genes},
volume = {14},
number = {4},
pages = {},
pmid = {37107559},
issn = {2073-4425},
mesh = {Humans ; Cell Line, Tumor ; *Neoplasm Recurrence, Local/pathology ; *Giant Cells/metabolism/pathology ; Polyploidy ; Computational Biology ; },
abstract = {Precision and organization govern the cell cycle, ensuring normal proliferation. However, some cells may undergo abnormal cell divisions (neosis) or variations of mitotic cycles (endopolyploidy). Consequently, the formation of polyploid giant cancer cells (PGCCs), critical for tumor survival, resistance, and immortalization, can occur. Newly formed cells end up accessing numerous multicellular and unicellular programs that enable metastasis, drug resistance, tumor recurrence, and self-renewal or diverse clone formation. An integrative literature review was carried out, searching articles in several sites, including: PUBMED, NCBI-PMC, and Google Academic, published in English, indexed in referenced databases and without a publication time filter, but prioritizing articles from the last 3 years, to answer the following questions: (i) "What is the current knowledge about polyploidy in tumors?"; (ii) "What are the applications of computational studies for the understanding of cancer polyploidy?"; and (iii) "How do PGCCs contribute to tumorigenesis?"},
}
MeSH Terms:
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Humans
Cell Line, Tumor
*Neoplasm Recurrence, Local/pathology
*Giant Cells/metabolism/pathology
Polyploidy
Computational Biology
RevDate: 2023-05-04
CmpDate: 2023-04-27
Evolution: Was the nuclear-to-cytoplasmic ratio a key factor in the origin of animal multicellularity?.
Current biology : CB, 33(8):R298-R300.
The ichthyosporean Sphaeroforma arctica, a protist closely related to animals, displays coenocytic development followed by cellularization and cell release. A new study reveals that the nuclear-to-cytoplasmic ratio drives cellularization in these fascinating organisms.
Additional Links: PMID-37098330
Publisher:
PubMed:
Citation:
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@article {pmid37098330,
year = {2023},
author = {Colgren, J and Burkhardt, P},
title = {Evolution: Was the nuclear-to-cytoplasmic ratio a key factor in the origin of animal multicellularity?.},
journal = {Current biology : CB},
volume = {33},
number = {8},
pages = {R298-R300},
doi = {10.1016/j.cub.2023.03.010},
pmid = {37098330},
issn = {1879-0445},
mesh = {Animals ; *Eukaryota ; *Mesomycetozoea ; Cytoplasm ; Cytosol ; Biological Evolution ; },
abstract = {The ichthyosporean Sphaeroforma arctica, a protist closely related to animals, displays coenocytic development followed by cellularization and cell release. A new study reveals that the nuclear-to-cytoplasmic ratio drives cellularization in these fascinating organisms.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Eukaryota
*Mesomycetozoea
Cytoplasm
Cytosol
Biological Evolution
RevDate: 2023-05-16
CmpDate: 2023-04-26
Hypothesis paper: the development of a regulatory layer in P2B autoinhibited Ca[2+]-ATPases may have facilitated plant terrestrialization and animal multicellularization.
Plant signaling & behavior, 18(1):2204284.
With the appearance of plants and animals, new challenges emerged. These multicellular eukaryotes had to solve for example the difficulties of multifaceted communication between cells and adaptation to new habitats. In this paper, we are looking for one piece of the puzzle that made the development of complex multicellular eukaryotes possible with a focus on regulation of P2B autoinhibited Ca[2+]-ATPases. P2B ATPases pump Ca[2+] out of the cytosol at the expense of ATP hydrolysis, and thereby maintain a steep gradient between the extra- and intracytosolic compartments which is utilized for Ca[2+]-mediated rapid cell signaling. The activity of these enzymes is regulated by a calmodulin (CaM)-responsive autoinhibitory region, which can be located in either termini of the protein, at the C-terminus in animals and at the N-terminus in plants. When the cytoplasmic Ca[2+] level reaches a threshold, the CaM/Ca[2+] complex binds to a calmodulin-binding domain (CaMBD) in the autoinhibitor, which leads to the upregulation of pump activity. In animals, protein activity is also controlled by acidic phospholipids that bind to a cytosolic portion of the pump. Here, we analyze the appearance of CaMBDs and the phospholipid-activating sequence and show that their evolution in animals and plants was independent. Furthermore, we hypothesize that different causes may have initiated the appearance of these regulatory layers: in animals, it is linked to the appearance of multicellularity, while in plants it co-occurs with their water-to-land transition.
Additional Links: PMID-37096591
PubMed:
Citation:
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@article {pmid37096591,
year = {2023},
author = {Stéger, A and Palmgren, M},
title = {Hypothesis paper: the development of a regulatory layer in P2B autoinhibited Ca[2+]-ATPases may have facilitated plant terrestrialization and animal multicellularization.},
journal = {Plant signaling & behavior},
volume = {18},
number = {1},
pages = {2204284},
pmid = {37096591},
issn = {1559-2324},
mesh = {Animals ; *Adenosine Triphosphatases ; *Calmodulin/metabolism ; Protein Binding ; Calcium Signaling ; Calcium/metabolism ; },
abstract = {With the appearance of plants and animals, new challenges emerged. These multicellular eukaryotes had to solve for example the difficulties of multifaceted communication between cells and adaptation to new habitats. In this paper, we are looking for one piece of the puzzle that made the development of complex multicellular eukaryotes possible with a focus on regulation of P2B autoinhibited Ca[2+]-ATPases. P2B ATPases pump Ca[2+] out of the cytosol at the expense of ATP hydrolysis, and thereby maintain a steep gradient between the extra- and intracytosolic compartments which is utilized for Ca[2+]-mediated rapid cell signaling. The activity of these enzymes is regulated by a calmodulin (CaM)-responsive autoinhibitory region, which can be located in either termini of the protein, at the C-terminus in animals and at the N-terminus in plants. When the cytoplasmic Ca[2+] level reaches a threshold, the CaM/Ca[2+] complex binds to a calmodulin-binding domain (CaMBD) in the autoinhibitor, which leads to the upregulation of pump activity. In animals, protein activity is also controlled by acidic phospholipids that bind to a cytosolic portion of the pump. Here, we analyze the appearance of CaMBDs and the phospholipid-activating sequence and show that their evolution in animals and plants was independent. Furthermore, we hypothesize that different causes may have initiated the appearance of these regulatory layers: in animals, it is linked to the appearance of multicellularity, while in plants it co-occurs with their water-to-land transition.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Adenosine Triphosphatases
*Calmodulin/metabolism
Protein Binding
Calcium Signaling
Calcium/metabolism
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