scholarly journals Evolutionary assembly patterns of prokaryotic genomes

2015 ◽  
Author(s):  
Maximilian O. Press ◽  
Christine Queitsch ◽  
Elhanan Borenstein
Keyword(s):  
Evolutionary Constraints ◽  
Historical Contingency ◽  
Phenotypic Characters ◽  
Functional Relationships ◽  
Evolutionary Innovation ◽  
Gene Level ◽  
Prokaryotic Genomes ◽  
Evolutionary Paths ◽  
Evolution Of Proteins ◽  
Sequence Substitution

AbstractEvolutionary innovation must occur in the context of some genomic background, which limits available evolutionary paths. For example, protein evolution by sequence substitution is constrained by epistasis between residues. In prokaryotes, evolutionary innovation frequently happens by macrogenomic events such as horizontal gene transfer (HGT). Previous work has suggested that HGT can be influenced by ancestral genomic content, yet the extent of such gene-level constraints has not yet been systematically characterized. Here, we evaluated the evolutionary impact of such constraints in prokaryotes, using probabilistic ancestral reconstructions from 634 extant prokaryotic genomes and a novel framework for detecting evolutionary constraints on HGT events. We identified 8,228 directional dependencies between genes, and demonstrated that many such dependencies reflect known functional relationships, including, for example, evolutionary dependencies of the photosynthetic enzyme RuBisCO. Modeling all dependencies as a network, we adapted an approach from graph theory to establish chronological precedence in the acquisition of different genomic functions. Specifically, we demonstrated that specific functions tend to be gained sequentially, suggesting that evolution in prokaryotes is governed by functional assembly patterns. Finally, we showed that these dependencies are universal rather than clade-specific and are often sufficient for predicting whether or not a given ancestral genome will acquire specific genes. Combined, our results indicate that evolutionary innovation via HGT is profoundly constrained by epistasis and historical contingency, similar to the evolution of proteins and phenotypic characters, and suggest that the emergence of specific metabolic and pathological phenotypes in prokaryotes can be predictable from current genomes.

scholarly journals Robustness by intrinsically disordered C-termini and translational readthrough

2018 ◽  
Vol 46 (19) ◽  
pp. 10184-10194 ◽  
Author(s):  
April Snofrid Kleppe ◽  
Erich Bornberg-Bauer
Keyword(s):  
High Frequency ◽  
Ribosomal Subunit ◽  
Conformational Flexibility ◽  
Ribosome Profiling ◽  
Protein Isoforms ◽  
Evolutionary Constraints ◽  
Protein Chain ◽  
Intrinsically Disordered ◽  
Translational Readthrough ◽  
Evolutionary Paths

Abstract During protein synthesis genetic instructions are passed from DNA via mRNA to the ribosome to assemble a protein chain. Occasionally, stop codons in the mRNA are bypassed and translation continues into the untranslated region (3′-UTR). This process, called translational readthrough (TR), yields a protein chain that becomes longer than would be predicted from the DNA sequence alone. Protein sequences vary in propensity for translational errors, which may yield evolutionary constraints by limiting evolutionary paths. Here we investigated TR in Saccharomyces cerevisiae by analysing ribosome profiling data. We clustered proteins as either prone or non-prone to TR, and conducted comparative analyses. We find that a relatively high frequency (5%) of genes undergo TR, including ribosomal subunit proteins. Our main finding is that proteins undergoing TR are highly expressed and have a higher proportion of intrinsically disordered C-termini. We suggest that highly expressed proteins may compensate for the deleterious effects of TR by having intrinsically disordered C-termini, which may provide conformational flexibility but without distorting native function. Moreover, we discuss whether minimizing deleterious effects of TR is also enabling exploration of the phenotypic landscape of protein isoforms.

The development of coronary vascularization

2018 ◽  
Author(s):  
Robert J. Tomanek ◽  
Adriana A. Silva Pires-Gomes ◽  
José Maria Pérez-Pomares
Keyword(s):  
Myocardial Infarction ◽  
Vascular System ◽  
Current Knowledge ◽  
Evolutionary Constraints ◽  
Myocardial Performance ◽  
Evolutionary Innovation ◽  
Cell Sources ◽  
Multiple Cell ◽  
Coronary Blood Vessels ◽  
Molecular Components

The coronary vascular system is a complex network of arteries, veins, and capillaries that supports myocardial performance, a topic previously reviewed by other authors. Disruption of coronary blood vessel form and/or function can underlie severe congenital and acquired cardiovascular conditions, from myocardial infarction to sudden death. Coronary blood vessels are an evolutionary innovation of vertebrates and form from multiple cell sources. Accordingly, the developmental complexity of coronary vessel morphogenesis is likely to reflect evolutionary constraints, as well as to explain the origins of coronary congenital anomalies (CCAs). In this chapter we summarize the current knowledge on coronary vascular development and identify the essential mechanistic cellular and molecular components of coronary morphogenesis. We will also provide plausible developmental explanations for some relevant CCAs.

scholarly journals Metabolic resilience is encoded in genome plasticity

2021 ◽  
Author(s):  
Leandro Z. Agudelo ◽  
Rémy V Tuyéras ◽  
Claudia Llinares ◽  
Alvaro Morcuende ◽  
Yongjin Park ◽  
...  
Keyword(s):  
Transcriptional Control ◽  
Functional Divergence ◽  
Resource Conservation ◽  
Genome Plasticity ◽  
Amino Acid Residues ◽  
Functional Relationships ◽  
Evolutionary Innovation ◽  
Disease Variant ◽  
Burst Kinetics

Metabolism plays a central role in evolution, as resource conservation is a selective pressure for fitness and survival. Resource-driven adaptations offer a good model to study evolutionary innovation more broadly. It remains unknown how resource-driven optimization of genome function integrates chromatin architecture with transcriptional phase transitions. Here we show that tuning of genome architecture and heterotypic transcriptional condensates mediate resilience to nutrient limitation. Network genomic integration of phenotypic, structural, and functional relationships reveals that fat tissue promotes organismal adaptations through metabolic acceleration chromatin domains and heterotypic PGC1A condensates. We find evolutionary innovation in several dimensions; low conservation of amino acid residues within protein disorder regions, nonrandom chromatin location of metabolic acceleration domains, condensate-chromatin stability through cis-regulatory archoring and encoding of genome plasticity in radial chromatin organization. We show that environmental tuning of these adaptations leads to fasting endurance, through efficient nuclear compartmentalization of lipid metabolic regions, and, locally, human-specific burst kinetics of lipid cycling genes. This process reduces oxidative stress, and fatty-acid mediated cellular acidification, enabling endurance of condensate chromatin conformations. Comparative genomics of genetic and diet perturbations reveal mammalian convergence of phenotype and structural relationships, along with loss of transcriptional control by diet-induced obesity. Further, we find that radial transcriptional organization is encoded in functional divergence of metabolic disease variant-hubs, heterotypic condensate composition, and evolutionary tuned protein residues sensing metabolic variation. During fuel restriction, these features license the formation of large heterotypic condensates that buffer proton excess, and shift viscoelasticity for condensate endurance. This mechanism maintains physiological pH, reduces pH-resilient inflammatory gene programs, and enables genome plasticity through transcriptionally driven cell-specific chromatin contacts. In vivo manipulation of this circuit promotes fasting-like adaptations with heterotypic nuclear compartments, metabolic and cell-specific homeostasis. In sum, we uncover here a general principle by which transcription uses environmental fluctuations for genome function, and demonstrate how resource conservation optimizes transcriptional self-organization through robust feedback integrators, highlighting obesity as an inhibitor of genome plasticity relevant for many diseases.

scholarly journals Predictability of Genetic Interactions from Functional Gene Modules

2016 ◽  
Author(s):  
Jonathan H. Young ◽  
Edward M. Marcotte
Keyword(s):  
Web Application ◽  
Genetic Interaction ◽  
Homo Sapiens ◽  
Interaction Network ◽  
Genetic Interactions ◽  
Functional Relationships ◽  
Therapy Targets ◽  
Genetic Interaction Network ◽  
Gene Level ◽  
Interaction Partners

AbstractCharacterizing genetic interactions is crucial to understanding cellular and organismal response to gene-level perturbations. Such knowledge can inform the selection of candidate disease therapy targets. Yet experimentally determining whether genes interact is technically non-trivial and time-consuming. High-fidelity prediction of different classes of genetic interactions in multiple organisms would substantially alleviate this experimental burden. Under the hypothesis that functionally-related genes tend to share common genetic interaction partners, we evaluate a computational approach to predict genetic interactions in Homo sapiens, Drosophila melanogaster, and Saccharomyces cerevisiae. By leveraging knowledge of functional relationships between genes, we cross-validate predictions on known genetic interactions and observe high-predictive power of multiple classes of genetic interactions in all three organisms. Additionally, our method suggests high-confidence candidate interaction pairs that can be directly experimentally tested. A web application is provided for users to query genes for predicted novel genetic interaction partners. Finally, by subsampling the known yeast genetic interaction network, we found that novel genetic interactions are predictable even when knowledge of currently known interactions is minimal.

scholarly journals The role of evolutionary selection in the dynamics of protein structure evolution

2016 ◽  
Author(s):  
Amy I. Gilson ◽  
Ahmee Marshall-Christensen ◽  
Jeong-Mo Choi ◽  
Eugene I. Shakhnovich
Keyword(s):  
Protein Structure ◽  
Sequence Divergence ◽  
Divergent Evolution ◽  
Structure Evolution ◽  
Linear Sequence ◽  
Structure Relationship ◽  
Ancient Proteins ◽  
Evolutionary Paths ◽  
Evolutionary Simulations ◽  
Evolution Of Proteins

AbstractHomology modeling is a powerful tool for predicting a protein’s structure. This approach is successful because proteins whose sequences are only 30% identical still adopt the same structure, while structure similarity rapidly deteriorates beyond the 30% threshold. By studying the divergence of protein structure as sequence evolves in real proteins and in evolutionary simulations, we show that this non-linear sequence-structure relationship emerges as a result of selection for protein folding stability in divergent evolution. Fitness constraints prevent the emergence of unstable protein evolutionary intermediates thereby enforcing evolutionary paths that preserve protein structure despite broad sequence divergence. However on longer time scales, evolution is punctuated by rare events where the fitness barriers obstructing structure evolution are overcome and discovery of new structures occurs. We outline biophysical and evolutionary rationale for broad variation in protein family sizes, prevalence of compact structures among ancient proteins and more rapid structure evolution of proteins with lower packing density.

scholarly journals Metabolic resilience is encoded in genome plasticity

2021 ◽  
Author(s):  
Leandro Agudelo ◽  
Remy Tuyeras ◽  
Claudia Llinares ◽  
Alvaro Morcuende ◽  
Yongjin Park ◽  
...  
Keyword(s):  
Transcriptional Control ◽  
Functional Divergence ◽  
Resource Conservation ◽  
Genome Plasticity ◽  
Amino Acid Residues ◽  
Functional Relationships ◽  
Evolutionary Innovation ◽  
Disease Variant ◽  
Burst Kinetics

Abstract Metabolism plays a central role in evolution, as resource conservation is a selective pressure for fitness and survival. Resource-driven adaptations offer a good model to study evolutionary innovation more broadly. It remains unknown how resource-driven optimization of genome function integrates chromatin architecture with transcriptional phase transitions. Here we show that tuning of genome architecture and heterotypic transcriptional condensates mediate resilience to nutrient limitation. Network genomic integration of phenotypic, structural, and functional relationships reveals that fat tissue promotes organismal adaptations through metabolic acceleration chromatin domains and heterotypic PGC1A condensates. We find evolutionary adaptations in several dimensions; low conservation of amino acid residues within protein disorder regions, nonrandom chromatin location of metabolic acceleration domains, condensate-chromatin stability through cis-regulatory anchoring and encoding of genome plasticity in radial chromatin organization. We show that environmental tuning of these adaptations leads to fasting endurance, through efficient nuclear compartmentalization of lipid metabolic regions, and, locally, human-specific burst kinetics of lipid cycling genes. This process reduces oxidative stress, and fatty-acid mediated cellular acidification, enabling endurance of condensate chromatin conformations. Comparative genomics of genetic and diet perturbations reveal mammalian convergence of phenotype and structural relationships, along with loss of transcriptional control by diet-induced obesity. Further, we find that radial transcriptional organization is encoded in functional divergence of metabolic disease variant-hubs, heterotypic condensate composition, and protein residues sensing metabolic variation. During fuel restriction, these features license the formation of large heterotypic condensates that buffer proton excess, and shift viscoelasticity for condensate endurance. This mechanism maintains physiological pH, reduces pH-resilient inflammatory gene programs, and enables genome plasticity through transcriptionally driven cell-specific chromatin contacts. In vivo manipulation of this circuit promotes fasting-like adaptations with heterotypic nuclear compartments, metabolic and cell-specific homeostasis. In sum, we uncover here a general principle by which transcription uses environmental fluctuations for genome function, and demonstrate how resource conservation optimizes transcriptional self-organization through robust feedback integrators, highlighting obesity as an inhibitor of genome plasticity relevant for many diseases.

Three-dimensional organization and functional relationships of endocytotic compartments in pig intestinal epithelial cells

1992 ◽  
Vol 50 (1) ◽  
pp. 576-577
Author(s):  
Julian P. Heath ◽  
Buford L. Nichols ◽  
László G. Kömüves
Keyword(s):  
Electron Microscopy ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Three Dimensional ◽  
Intestinal Epithelial ◽  
Cell Surfaces ◽  
Basal Surface ◽  
Functional Relationships

The newborn pig intestine is adapted for the rapid and efficient absorption of nutrients from colostrum. In enterocytes, colostral proteins are taken up into an apical endocytotic complex of channels that transports them to target organelles or to the basal surface for release into the circulation. The apical endocytotic complex of tubules and vesicles clearly is a major intersection in the routes taken by vesicles trafficking to and from the Golgi, lysosomes, and the apical and basolateral cell surfaces.Jejunal tissues were taken from piglets suckled for up to 6 hours and prepared for electron microscopy and immunocytochemistry as previously described.

Homology, Genes, and Evolutionary Innovation

2014 ◽  
Author(s):  
Günter P. Wagner
Keyword(s):  
Evolutionary Biology ◽  
Regulatory Networks ◽  
Biological Diversity ◽  
Cell Types ◽  
Origin And Evolution ◽  
Major Transitions ◽  
Form And Function ◽  
Historical Continuity ◽  
Evolutionary Innovation ◽  
Character Identity

Homology—a similar trait shared by different species and derived from common ancestry, such as a seal's fin and a bird's wing—is one of the most fundamental yet challenging concepts in evolutionary biology. This book provides the first mechanistically based theory of what homology is and how it arises in evolution. The book argues that homology, or character identity, can be explained through the historical continuity of character identity networks—that is, the gene regulatory networks that enable differential gene expression. It shows how character identity is independent of the form and function of the character itself because the same network can activate different effector genes and thus control the development of different shapes, sizes, and qualities of the character. Demonstrating how this theoretical model can provide a foundation for understanding the evolutionary origin of novel characters, the book applies it to the origin and evolution of specific systems, such as cell types; skin, hair, and feathers; limbs and digits; and flowers. The first major synthesis of homology to be published in decades, this book reveals how a mechanistically based theory can serve as a unifying concept for any branch of science concerned with the structure and development of organisms, and how it can help explain major transitions in evolution and broad patterns of biological diversity.

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