Evolutionary dynamics, epistatic interactions, and biological information

2010 ◽  
Vol 266 (4) ◽  
pp. 584-594 ◽  
Author(s):  
Christopher C. Strelioff ◽  
Richard E. Lenski ◽  
Charles Ofria
Keyword(s):  
Evolutionary Dynamics ◽  
Biological Information ◽  
Epistatic Interactions

scholarly journals The distribution of epistasis on simple fitness landscapes

2018 ◽  
Author(s):  
Christelle Fraïsse ◽  
John J. Welch
Keyword(s):  
Evolutionary Dynamics ◽  
Fitness Landscape ◽  
Null Model ◽  
Large Data ◽  
Fitness Landscapes ◽  
Mutational Bias ◽  
Data Set ◽  
Epistatic Interactions ◽  
Standing Variation ◽  
Mean And Variance

AbstractFitness interactions between mutations can influence a population’s evolution in many different ways. While epistatic effects are difficult to measure precisely, important information about the overall distribution is captured by the mean and variance of log fitnesses for individuals carrying different numbers of mutations. We derive predictions for these quantities from simple fitness landscapes, based on models of optimizing selection on quantitative traits. We also explore extensions to the models, including modular pleiotropy, variable effects sizes, mutational bias, and maladaptation of the wild-type. We illustrate our approach by reanalysing a large data set of mutant effects in a yeast snoRNA. Though characterized by some strong epistatic interactions, these data give a good overall fit to the non-epistatic null model, suggesting that epistasis might have little effect on the evolutionary dynamics in this system. We also show how the amount of epistasis depends on both the underlying fitness landscape, and the distribution of mutations, and so it is expected to vary in consistent ways between new mutations, standing variation, and fixed mutations.

scholarly journals Positive selection of ORF3a and ORF8 genes drives the evolution of SARS-CoV-2 during the 2020 COVID-19 pandemic

2020 ◽  
Author(s):  
Lauro Velazquez-Salinas ◽  
Selene Zarate ◽  
Samantha Eberl ◽  
Douglas P. Gladue ◽  
Isabel Novella ◽  
...  
Keyword(s):  
Public Health ◽  
Positive Selection ◽  
Evolutionary Dynamics ◽  
Full Length ◽  
Accessory Proteins ◽  
The Novel ◽  
Phylogenetic Groups ◽  
Epistatic Interactions ◽  
Genetic Mechanisms ◽  
Selection Of

AbstractIn this study, we analyzed full-length SARS-CoV-2 genomes from multiple countries to determine early trends in the evolutionary dynamics of the novel COVID-19 pandemic. Results indicated SARS-CoV-2 evolved early into at least three phylogenetic groups, characterized by positive selection at specific residues of the accessory proteins OFR3a and ORF8a. We also report evidence of epistatic interactions among sites in the genome that may be important in the generation of variants adapted to humans. These observations might impact not only public health, but also suggest more studies are needed to understand the genetic mechanisms that may affect the development of therapeutic and preventive tools, like antivirals and vaccines.

scholarly journals Synergistic epistasis of the deleterious effects of transposable elements

Genetics ◽  
2021 ◽  
Author(s):  
Yuh Chwen G Lee
Keyword(s):  
Transposable Elements ◽  
Copy Number ◽  
Evolutionary Dynamics ◽  
Purifying Selection ◽  
Epistatic Interactions ◽  
Deleterious Alleles ◽  
Mixed Support ◽  
Genetic Signal ◽  
Outstanding Question ◽  
Repulsion Linkage

Abstract The replicative nature and generally deleterious effects of transposable elements (TEs) raise an outstanding question about how TE copy number is stably contained in host populations. Classic theoretical analyses predict that, when the decline in fitness due to each additional TE insertion is greater than linear, or when there is synergistic epistasis, selection against TEs can result in a stable equilibrium of TE copy number. While several mechanisms are predicted to yield synergistic deleterious effects of TEs, we lack empirical investigations of the presence of such epistatic interactions. Purifying selection with synergistic epistasis generates repulsion linkage between deleterious alleles. We investigated this population genetic signal in the likely ancestral Drosophila melanogaster population and found evidence supporting the presence of synergistic epistasis among TE insertions, especially TEs expected to exert large fitness impacts. Even though synergistic epistasis of TEs has been predicted to arise through ectopic recombination and TE-mediated epigenetic silencing mechanisms, we only found mixed support for the associated predictions. We observed signals of synergistic epistasis for a large number of TE families, which is consistent with the expectation that such epistatic interaction mainly happens among copies of the same family. Curiously, significant repulsion linkage was also found among TE insertions from different families, suggesting the possibility that synergism of TEs’ deleterious fitness effects could arise above the family level and through mechanisms similar to those of simple mutations. Our findings set the stage for investigating the prevalence and importance of epistatic interactions in the evolutionary dynamics of TEs.

scholarly journals Synergistic epistasis of the deleterious effects of transposable elements

2021 ◽  
Author(s):  
Grace Yuh Chwen Lee
Keyword(s):  
Transposable Elements ◽  
Copy Number ◽  
Evolutionary Dynamics ◽  
Purifying Selection ◽  
Epistatic Interactions ◽  
Ectopic Recombination ◽  
Epigenetic Effects ◽  
Deleterious Alleles ◽  
Genetic Signal ◽  
Outstanding Question

The replicative nature and generally deleterious effects of transposable elements (TEs) give rise to an outstanding question about how TE copy number is stably contained in host populations. Classic theoretical analyses predict that, when the decline in fitness due to each additional TE insertion is greater than linear, or when there is synergistic epistasis, selection against TEs can result in a stable equilibrium of TE copy number. While several mechanisms are predicted to yield synergistic deleterious effects of TEs, we lack empirical investigations of the presence of such epistatic interactions. Purifying selection with synergistic epistasis generates repulsion linkage between deleterious alleles and, accordingly, an underdispersed distribution for the number of deleterious mutations among individuals. We investigated this population genetic signal in an African Drosophila melanogaster population and found evidence for synergistic epistasis among TE insertions, especially those expected to have large fitness impacts. Curiously, even though ectopic recombination has long been predicted to generate nonlinear fitness decline with increased TE copy number, TEs predicted to suffer higher rates of ectopic recombination are not more likely to be underdispersed. On the other hand, underdispersed TE families are more likely to show signatures of deleterious epigenetic effects and stronger ping-pong signals of piRNA amplification, a hypothesized source from which synergism of TE-mediated epigenetic effects arises. Our findings set the stage for investigating the importance of epistatic interactions in the evolutionary dynamics of TEs.

scholarly journals The ups and downs of amino acid co-evolution: evolutionary Stokes and anti-Stokes shifts

2020 ◽  
Author(s):  
Noor Youssef ◽  
Edward Susko ◽  
Andrew Roger ◽  
Joseph Bielawski
Keyword(s):  
Amino Acid ◽  
Evolutionary Dynamics ◽  
Stokes Shift ◽  
Conclusive Evidence ◽  
Adaptive Responses ◽  
Epistatic Interactions ◽  
Amino Acid Propensity ◽  
Evolutionary Paths ◽  
Anti Stokes ◽  
Stokes Shifts

Abstract The most fundamental form of epistasis occurs between residues within a protein. Epistatic interactions can have significant consequences for evolutionary dynamics. For example, a substitution to a deleterious amino acid may be compensated for by replacements at other sites which increase its propensity (a function of its average fitness) over time - this is the evolutionary Stokes shift. We discovered that an opposite trend -the decrease in amino acid propensity with time- can also occur via the same epistatic dynamics. We define this novel and pervasive phenomenon as the evolutionary anti-Stokes shift. Our extensive simulations of three natural proteins show that evolutionary Stokes and anti-Stokes shifts occur with similar frequencies and magnitudes across the protein. This highlights that decreasing amino acid propensities, on their own, are not conclusive evidence of adaptive responses to a changing environment. We find that stabilizing substitutions are often permissive (i.e., expand potential evolutionary paths) whereas destabilizing substitutions are restrictive. We show how these dynamics explain the variations in amino acid propensities associated with both evolutionary shifts in propensities.

Fitness Landscape Models

2003 ◽  
Author(s):  
M. E. J. Newman ◽  
R. G. Palmer
Keyword(s):  
Statistical Physics ◽  
Evolutionary Dynamics ◽  
Fitness Landscape ◽  
Real Life ◽  
Extinction Rate ◽  
Epistatic Interactions ◽  
Nk Model ◽  
Energy Models ◽  
Landscape Models ◽  
A Genome

Kauffman (1993, 1995; Kauffman and Levin 1987; Kauffman and Johnsen 1991) has proposed and studied in depth a class of models referred to as NK models, which are models of random fitness landscapes on which one can implement a variety of types of evolutionary dynamics and study the development and interaction of species. (The letters N and K do not stand for anything; they are the names of parameters in the model.) Based on the results of extensive simulations of NK models, Kauffman and co-workers have suggested a number of possible connections between the dynamics of evolution and the extinction rate. To a large extent it is this work which has sparked recent interest in biotic mechanisms for mass extinction. In this chapter we review Kauffman's work in detail. An NK model is a model of a single rugged landscape, which is similar in construction to the spin-glass models of statistical physics (Fischer and Hertz 1991), particularly p-spin models (Derrida 1980) and random energy models (Derrida 1981). Used as a model of species fitness the NK model maps the states of a model genome onto a scalar fitness W. This is a simplification of what happens in real life, where the genotype is first mapped onto phenotype and only then onto fitness. However, it is a useful simplification which makes simulation of the model for large systems tractable. As long as we bear in mind that this simplification has been made, the model can still teach us many useful things. The NK model is a model of a genome with N genes. Each gene has A alleles. In most of Kauffman's studies of the model he used A = 2, a binary genetic code, but his results are not limited to this case. The model also includes epistatic interactions between genes—interactions whereby the state of one gene affects the contribution of another to the overall fitness of the species. In fact, it is these epistatic interactions which are responsible for the ruggedness of the fitness landscape.

scholarly journals The ups and downs of amino acid co-evolution: evolutionary Stokes and anti-Stokes shifts

2020 ◽  
Author(s):  
Noor Youssef ◽  
Edward Susko ◽  
Andrew J. Roger ◽  
Joseph P. Bielawski
Keyword(s):  
Amino Acid ◽  
Evolutionary Dynamics ◽  
Stokes Shift ◽  
Conclusive Evidence ◽  
Adaptive Responses ◽  
Epistatic Interactions ◽  
Amino Acid Propensity ◽  
Evolutionary Paths ◽  
Anti Stokes ◽  
Stokes Shifts

AbstractThe most fundamental form of epistasis occurs between residues within a protein. Epistatic interactions can have significant consequences for evolutionary dynamics. For example, a substitution to a deleterious amino acid may be compensated for by replacements at other sites which increase its propensity (a function of its average fitness) over time - this is the evolutionary Stokes shift. We discovered that an opposite trend -the decrease in amino acid propensity with time-can also occur via the same epistatic dynamics. We define this novel and pervasive phenomenon as the evolutionary anti-Stokes shift. Our extensive simulations of three natural proteins show that evolutionary Stokes and anti-Stokes shifts occur with similar frequencies and magnitudes across the protein. This high-lights that decreasing amino acid propensities, on their own, are not conclusive evidence of adaptive responses to a changing environment. We find that stabilizing substitutions are often permissive (i.e., expand potential evolutionary paths) whereas destabilizing substitutions are restrictive. We show how these dynamics explain the variations in amino acid propensities associated with both evolutionary shifts in propensities.

Multilocus Analysis of Genetic Susceptibility to Myocardial Infarction in Russians: Replication Study

Acta Naturae ◽  
2017 ◽  
Vol 9 (4) ◽  
pp. 74-83
Author(s):  
N. G. Kukava ◽  
B. V. Titov ◽  
G. J. Osmak ◽  
N. A. Matveeva ◽  
O. G. Kulakova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Genetic Markers ◽  
Prognostic Significance ◽  
Cumulative Effect ◽  
Mthfr Gene ◽  
Composite Model ◽  
Replication Study ◽  
Epistatic Interactions ◽  
Multilocus Analysis ◽  
Lipid Metabolism Genes

In search of genetic markers of myocardial infarction (MI) risk, which have prognostic significance for Russians, we performed a replication study of MI association with genetic variants of PCSK9 (rs562556), APOE (epsilon polymorphism, rs7412 and rs429358), LPL (rs320), MTHFR (rs1801133), eNOS (rs2070744), and the 9p21 region (rs1333049) in 405 patients with MI and 198 controls. Significant MI association was observed with variants of the lipid metabolism genes (PCSK9, APOE and LPL), and of eNOS. The SNPs in the MTHFR gene and the 9p21 region were not significantly associated with MI one by one but were included in several different MI-associated allelic combinations identified by multilocus analysis. Since we have not revealed nonlinear epistatic interactions between the components of the identified combinations, we postulate that the cumulative effect of genes that form a combination arises from the summation of their small independent contributions. The prognostic significance of the additive composite model built from the PCSK9, APOE, LPL, and eNOS genes as genetic markers was assessed using ROC analysis. After we included these markers in the previously published composite model of individual genetic risk of MI, the prognostic efficacy in our sample reached AUC = 0.676. However, the results obtained in this study certainly need to be replicated in an independent sample of Russians.

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