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The exact distributions of F(IS) under partial asexuality in small finite populations with mutation.

ABSTRACT: Reproductive systems like partial asexuality participate to shape the evolution of genetic diversity within populations, which is often quantified by the inbreeding coefficient F IS. Understanding how those mating systems impact the possible distributions of F IS values in theoretical populations helps to unravel forces shaping the evolution of real populations. We proposed a population genetics model based on genotypic states in a finite population with mutation. For populations with less than 400 individuals, we assessed the impact of the rates of asexuality on the full exact distributions of F IS, the probabilities of positive and negative F IS, the probabilities of fixation and the probabilities to observe changes in the sign of F IS over one generation. After an infinite number of generations, we distinguished three main patterns of effects of the rates of asexuality on genetic diversity that also varied according to the interactions of mutation and genetic drift. Even rare asexual events in mainly sexual populations impacted the balance between negative and positive F IS and the occurrence of extreme values. It also drastically modified the probability to change the sign of F IS value at one locus over one generation. When mutation prevailed over genetic drift, increasing rates of asexuality continuously increased the variance of F IS that reached its highest value in fully asexual populations. In consequence, even ancient asexual populations showed the entire F IS spectrum, including strong positive F IS. The prevalence of heterozygous loci only occurred in full asexual populations when genetic drift dominated.

SUBMITTER: Stoeckel S

PROVIDER: S-EPMC3897417 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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The exact distributions of F(IS) under partial asexuality in small finite populations with mutation.

Stoeckel Solenn S Masson Jean-Pierre JP

PloS one 20140121 1

Reproductive systems like partial asexuality participate to shape the evolution of genetic diversity within populations, which is often quantified by the inbreeding coefficient F IS. Understanding how those mating systems impact the possible distributions of F IS values in theoretical populations helps to unravel forces shaping the evolution of real populations. We proposed a population genetics model based on genotypic states in a finite population with mutation. For populations with less than ...[more]

PMID: 24465510

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Project description:Reproduction is inherently risky, in part because genomic replication can introduce new mutations that are usually deleterious toward fitness. This risk is especially severe for organisms whose genomes replicate "semi-conservatively," e.g. viruses and bacteria, where no master copy of the genome is preserved. Lethal mutagenesis refers to extinction of populations due to an unbearably high mutation rate (U), and is important both theoretically and clinically, where drugs can extinguish pathogens by increasing their mutation rate. Previous theoretical models of lethal mutagenesis assume infinite population size (N). However, in addition to high U, small N can accelerate extinction by strengthening genetic drift and relaxing selection. Here, we examine how the time until extinction depends jointly on N and U. We first analytically compute the mean time until extinction (τ) in a simplistic model where all mutations are either lethal or neutral. The solution motivates the definition of two distinct regimes: a survival phase and an extinction phase, which differ dramatically in both how τ scales with N and in the coefficient of variation in time until extinction. Next, we perform stochastic population-genetics simulations on a realistic fitness landscape that both (i) features an epistatic distribution of fitness effects that agrees with experimental data on viruses and (ii) is based on the biophysics of protein folding. More specifically, we assume that mutations inflict fitness penalties proportional to the extent that they unfold proteins. We find that decreasing N can cause phase transition-like behavior from survival to extinction, which motivates the concept of "lethal isolation." Furthermore, we find that lethal mutagenesis and lethal isolation interact synergistically, which may have clinical implications for treating infections. Broadly, we conclude that stably folded proteins are only possible in ecological settings that support sufficiently large populations.

Dataset Information

The exact distributions of F(IS) under partial asexuality in small finite populations with mutation.

Publications

The exact distributions of F(IS) under partial asexuality in small finite populations with mutation.

Similar Datasets

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