ADAPTIVE EVOLUTION OF ASEXUAL POPULATIONS UNDER MULLER'S RATCHET

Evolution ◽  
2004 ◽  
Vol 58 (7) ◽  
pp. 1403 ◽  
Author(s):  
Doris Bachtrog ◽  
Isabel Gordo
Keyword(s):  
Adaptive Evolution ◽  
Muller's Ratchet ◽  
Muller’S Ratchet ◽  
Asexual Populations

scholarly journals The advance of Muller's ratchet in a haploid asexual population: approximate solutions based on diffusion theory

1993 ◽  
Vol 61 (3) ◽  
pp. 225-231 ◽  
Author(s):  
Wolfgang Stephan ◽  
Lin Chao ◽  
Joanne Guna Smale
Keyword(s):  
Diffusion Theory ◽  
Large Population ◽  
Approximate Solutions ◽  
Diffusion Approximations ◽  
Asexual Population ◽  
Muller's Ratchet ◽  
Expected Time ◽  
Equilibrium Size ◽  
Muller’S Ratchet ◽  
Asexual Populations

SummaryAsexual populations experiencing random genetic drift can accumulate an increasing number of deleterious mutations, a process called Muller's ratchet. We present here diffusion approximations for the rate at which Muller's ratchet advances in asexual haploid populations. The most important parameter of this process is n0 = N e−U/s, where N is population size, U the genomic mutation rate and s the selection coefficient. In a very large population, n0 is the equilibrium size of the mutation-free class. We examined the case n0 > 1 and developed one approximation for intermediate values of N and s and one for large values of N and s. For intermediate values, the expected time at which the ratchet advances increases linearly with n0. For large values, the time increases in a more or less exponential fashion with n0. In addition to n0, s is also an important determinant of the speed of the ratchet. If N and s are intermediate and n0 is fixed, we find that increasing s accelerates the ratchet. In contrast, for a given n0, but large N and s, increasing s slows the ratchet. Except when s is small, results based on our approximations fit well those from computer simulations.

scholarly journals Defying Muller’s Ratchet: Ancient Heritable Endobacteria Escape Extinction through Retention of Recombination and Genome Plasticity

mBio ◽  
2016 ◽  
Vol 7 (3) ◽  
Author(s):  
Mizue Naito ◽  
Teresa E. Pawlowska
Keyword(s):  
Mycorrhizal Fungi ◽  
Arbuscular Mycorrhizal ◽  
Genome Plasticity ◽  
Escape Extinction ◽  
Muller's Ratchet ◽  
Evolutionary Forces ◽  
Slightly Deleterious Mutations ◽  
Muller’S Ratchet ◽  
Asexual Populations ◽  
Host Generation

ABSTRACT   Heritable endobacteria, which are transmitted from one host generation to the next, are subjected to evolutionary forces that are different from those experienced by free-living bacteria. In particular, they suffer consequences of Muller’s ratchet, a mechanism that leads to extinction of small asexual populations due to fixation of slightly deleterious mutations combined with the random loss of the most-fit genotypes, which cannot be recreated without recombination. Mycoplasma-related endobacteria (MRE) are heritable symbionts of fungi from two ancient lineages, Glomeromycota (arbuscular mycorrhizal fungi) and Mucoromycotina . Previous studies revealed that MRE maintain unusually diverse populations inside their hosts and may have been associated with fungi already in the early Paleozoic. Here we show that MRE are vulnerable to genomic degeneration and propose that they defy Muller’s ratchet thanks to retention of recombination and genome plasticity. We suggest that other endobacteria may be capable of raising similar defenses against Muller’s ratchet.

scholarly journals Muller’s Ratchet in Asexual Populations Doomed to Extinction

2018 ◽  
Author(s):  
Logan Chipkin ◽  
Peter Olofsson ◽  
Ryan C. Daileda ◽  
Ricardo B. R. Azevedo
Keyword(s):  
Process Model ◽  
Population Decline ◽  
Extinction Time ◽  
Deleterious Mutations ◽  
Multitype Branching Process ◽  
Muller's Ratchet ◽  
Constant Size ◽  
Muller’S Ratchet ◽  
Asexual Populations ◽  
Mutational Meltdown

AbstractAsexual populations are expected to accumulate deleterious mutations through a process known as Muller’s Ratchet. Lynch, Gabriel, and colleagues have proposed that the Ratchet eventually results in a vicious cycle of mutation accumulation and population decline that drives populations to extinction. They called this phenomenon mutational meltdown. Here, we analyze the meltdown using a multitype branching process model where, in the presence of mutation, populations are doomed to extinction. We find that extinction occurs more quickly in small populations, experiencing a high deleterious mutation rate, and mutations with more severe deleterious effects. The effects of mutational parameters on extinction time in doomed populations differ from those on the severity of Muller’s Ratchet in populations of constant size. We also 1nd that mutational meltdown, although it does occur in our model, does not determine extinction time. Rather, extinction time is determined by the expected impact of deleterious mutations on fitness.

scholarly journals The constraints of finite size in asexual populations and the rate of the ratchet

1995 ◽  
Vol 66 (3) ◽  
pp. 241-253 ◽  
Author(s):  
Damian D. G. Gessler
Keyword(s):  
Negative Binomial ◽  
Finite Size ◽  
Mutation Accumulation ◽  
Necessary Condition ◽  
Mutation Pressure ◽  
Actual Distribution ◽  
Muller's Ratchet ◽  
State Strength ◽  
Muller’S Ratchet ◽  
Asexual Populations

SummaryAn analysis of mutation accumulation in finite, asexual populations shows that by modeling discrete individuals, a necessary condition for mutation–selection balance is often not met. It is found that over a wide parameter range (whenever N e−μ/s < 1, where N is the population size, μ is the genome-wide mutation rate, and s is the realized strength of selection), asexual populations will fail to achieve mutation–selection balance. This is specifically because the steady-state strength of selection on the best individuals is too weak to counter mutation pressure. The discrete nature of individuals means that if the equilibrium level of mutation and selection is such that less than one individual is expected in a class, then equilibration towards this level acts to remove the class. When applied to the classes with the fewest mutations, this drives mutation accumulation. This drive is in addition to the well-known identification of the stochastic loss of the best class as a mechanism for Muller's ratchet. Quantification of this process explains why the distribution of the number of mutations per individual can be markedly hypodispersed compared to the Poisson expectation. The actual distribution, when corrected for stochasticity between the best class and the mean, is akin to a shifted negative binomial. The parameterization of the distribution allows for an approximation for the rate of Muller's ratchet when N e−μ/s < 1. The analysis is extended to the case of variable selection coefficients where incoming mutations assume a distribution of deleterious effects. Under this condition, asexual populations accumulate mutations faster, yet may be able to survive longer, than previously estimated.

Muller’s ratchet of the Y chromosome with gene conversion

Genetics ◽  
2021 ◽  
Author(s):  
Takahiro Sakamoto ◽  
Hideki Innan
Keyword(s):  
Gene Duplication ◽  
Gene Conversion ◽  
Y Chromosome ◽  
Conversion Rate ◽  
Single Copy ◽  
Duplicated Genes ◽  
Fitness Effect ◽  
Muller's Ratchet ◽  
Y Chromosomes ◽  
Muller’S Ratchet

Abstract Muller’s ratchet is a process in which deleterious mutations are fixed irreversibly in the absence of recombination. The degeneration of the Y chromosome, and the gradual loss of its genes, can be explained by Muller’s ratchet. However, most theories consider single-copy genes, and may not be applicable to Y chromosomes, which have a number of duplicated genes in many species, which are probably undergoing concerted evolution by gene conversion. We developed a model of Muller’s ratchet to explore the evolution of the Y chromosome. The model assumes a non-recombining chromosome with both single-copy and duplicated genes. We used analytical and simulation approaches to obtain the rate of gene loss in this model, with special attention to the role of gene conversion. Homogenization by gene conversion makes both duplicated copies either mutated or intact. The former promotes the ratchet, and the latter retards, and we ask which of these counteracting forces dominates under which conditions. We found that the effect of gene conversion is complex, and depends upon the fitness effect of gene duplication. When duplication has no effect on fitness, gene conversion accelerates the ratchet of both single-copy and duplicated genes. If duplication has an additive fitness effect, the ratchet of single-copy genes is accelerated by gene duplication, regardless of the gene conversion rate, whereas gene conversion slows the degeneration of duplicated genes. Our results suggest that the evolution of the Y chromosome involves several parameters, including the fitness effect of gene duplication by increasing dosage and gene conversion rate.

scholarly journals Hitchhiking and epistasis give rise to cohort dynamics in adapting populations

2017 ◽  
Vol 114 (31) ◽  
pp. 8330-8335 ◽  
Author(s):  
Sean W. Buskirk ◽  
Ryan Emily Peace ◽  
Gregory I. Lang
Keyword(s):  
Adaptive Evolution ◽  
Driving Force ◽  
Parallel Evolution ◽  
Low Frequency ◽  
Target Size ◽  
Driver Mutations ◽  
Beneficial Mutations ◽  
Large Target ◽  
Asexual Populations ◽  
Comprehensive Study

Beneficial mutations are the driving force of adaptive evolution. In asexual populations, the identification of beneficial alleles is confounded by the presence of genetically linked hitchhiker mutations. Parallel evolution experiments enable the recognition of common targets of selection; yet these targets are inherently enriched for genes of large target size and mutations of large effect. A comprehensive study of individual mutations is necessary to create a realistic picture of the evolutionarily significant spectrum of beneficial mutations. Here we use a bulk-segregant approach to identify the beneficial mutations across 11 lineages of experimentally evolved yeast populations. We report that nearly 80% of detected mutations have no discernible effects on fitness and less than 1% are deleterious. We determine the distribution of driver and hitchhiker mutations in 31 mutational cohorts, groups of mutations that arise synchronously from low frequency and track tightly with one another. Surprisingly, we find that one-third of cohorts lack identifiable driver mutations. In addition, we identify intracohort synergistic epistasis between alleles of hsl7 and kel1, which arose together in a low-frequency lineage.

Amazon molly and Muller's ratchet

Nature ◽  
1995 ◽  
Vol 375 (6527) ◽  
pp. 111-112 ◽  
Author(s):  
Leo W. Beukeboom ◽  
Rolf P. Weinzierl ◽  
Nico K. Michiels
Keyword(s):  
Muller's Ratchet ◽  
Amazon Molly ◽  
Muller’S Ratchet
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