scholarly journals Sex, fitness decline and recombination – Muller’s ratchet vs. Ohta’s ratchet

2020 ◽  
Author(s):  
Yongsen Ruan ◽  
Haiyu Wang ◽  
Lingjie Zhang ◽  
Haijun Wen ◽  
Chung-I Wu
Keyword(s):  
Parameter Space ◽  
Asexual Population ◽  
Main Hypothesis ◽  
Muller's Ratchet ◽  
Restricted Parameter Space ◽  
Biological Phenomena ◽  
Muller’S Ratchet ◽  
Selection For ◽  
Driving Fitness ◽  
Special Case

AbstractIt is generally accepted that the absence of recombination reduces the efficacy of natural selection for, or against, mutations. A special case is Muller’s Ratchet (MR) whereby non-recombining genomes experience irreversible fitness decline due to the accumulation of deleterious mutations. MR has been a main hypothesis for sexual reproduction as well as many other biological phenomena. We now ask whether the fitness decline can indeed be stopped if an asexual population turns sexual to become recombining. The possible fitness decline under recombination is referred to as Ohta’s Ratchet (OR). In comparison, MR is more effective in driving fitness reduction than OR, but only in a restricted parameter space of mutation rate, population size and selection. Outside of this space, the two ratchets are equally effective or, alternatively, neither is sufficiently powerful. Furthermore, beneficial mutations can affect the population fitness, which may diverge between the two ratchets, but only in a small parameter space. Since recombination plays a limited role in driving fitness decline, the operation of MR could be far less common in nature than believed. A companion report (see Supplement) surveying the biological phenomena attributed to MR indeed suggests the alternative explanations to be generally more compelling.

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 Rapid fixation of deleterious alleles can be caused by Muller's ratchet

1997 ◽  
Vol 70 (1) ◽  
pp. 63-73 ◽  
Author(s):  
BRIAN CHARLESWORTH ◽  
DEBORAH CHARLESWORTH
Keyword(s):  
Analytical Approximation ◽  
Similar Process ◽  
Asexual Population ◽  
Single Chromosome ◽  
Muller's Ratchet ◽  
Analytical Approximations ◽  
Deleterious Alleles ◽  
Wide Range ◽  
Muller’S Ratchet ◽  
Parameter Values

Theoretical arguments are presented which suggest that each advance of Muller's ratchet in a haploid asexual population causes the fixation of a deleterious mutation at a single locus. A similar process operates in a diploid, fully asexual population under a wide range of parameter values, with respect to fixation within one of the two haploid genomes. Fixations of deleterious mutations in asexual species can thus be greatly accelerated in comparison with a freely recombining genome, if the ratchet is operating. In a diploid with segregation of a single chromosome, but no crossing over within the chromosome, the advance of the ratchet can be decoupled from fixation if mutations are sufficiently close to recessivity. A new analytical approximation for the rate of advance of the ratchet is proposed. Simulation results are presented that validate the assertions about fixation. The simulations show that none of the analytical approximations for the rate of advance of the ratchet are satisfactory when population size is large. The relevance of these results for evolutionary processes such as Y chromosome degeneration is discussed.

scholarly journals Muller's ratchet under epistatic selection.

Genetics ◽  
1994 ◽  
Vol 136 (4) ◽  
pp. 1469-1473 ◽  
Author(s):  
A S Kondrashov
Keyword(s):  
Previous Analysis ◽  
Random Drift ◽  
Asexual Population ◽  
Muller's Ratchet ◽  
Fitness Effects ◽  
Deleterious Alleles ◽  
Minimum Number ◽  
Muller’S Ratchet ◽  
Mean Fitness ◽  
Independent Effects

Abstract In a finite asexual population mean fitness may decrease by a process known as Muller's ratchet, which proceeds if all individuals with the minimum number of deleterious alleles are randomly lost. If these alleles have independent effects on fitness, previous analysis suggested that the rate of this decrease either remains constant or, if accumulation of mutations leads to the decline of the population size, grows. Here I show that this conclusion is quite sensitive to the assumption of independence. If deleterious alleles have synergistic fitness effects, then, as the ratchet advances, the frequency of the best available genotype will necessarily increase, making its loss less and less probable. As a result, sufficiently strong synergistic epistasis can effectively halt the action of Muller's ratchet. Instead of being driven extinct, a finite asexual population could then survive practically indefinitely, although with lower mean fitness than without random drift.

scholarly journals 053 CLONAL DECLINE IN HORTICULTURAL CROPS DUE TO MULLER'S RATCHET

HortScience ◽  
1994 ◽  
Vol 29 (5) ◽  
pp. 435e-435
Author(s):  
Neil O. Anderson ◽  
Peter D. Ascher
Keyword(s):  
Seed Set ◽  
Virus Titer ◽  
Sexual Cycle ◽  
Stunted Growth ◽  
Muller's Ratchet ◽  
Horticultural Crops ◽  
Muller’S Ratchet ◽  
Selection For ◽  
Sterile Seed ◽  
Disease Free

It should be possible to maintain horticultural clones unchanged forever through asexual generations, as commercial propagators and clonal repositories maintain clonal integrity, disease-free stock plants, or remove mutations. However, unintentional selection for nonhorticultural traits could still be occurring. Accumulations of such traits would be due to the operation of Muller's ratchet and include fertility losses, increases in virus titer, and stunted growth habit. In chrysanthemums, Dendranthema grandiflora. clones separated from sexual cycles for generations become increasingly sterile. Seed set across years, using coefficients of crossability (FCC/MCC), was examined for garden clones (forced through sexual cycles annually) and greenhouse clones (asexual cycles only). Garden clones 40 years old (54-101-11) had only depressed levels of fertility. In other cases (77-AM 3-17), the ratchet was reversed >1 sexual cycle. Greenhouse clones were often completely sterile since their propagation is primarily asexual.

scholarly journals Genetic Hitchhiking and the Evolution of Reduced Genetic Activity of the Y Sex Chromosome

Genetics ◽  
1987 ◽  
Vol 116 (1) ◽  
pp. 161-167
Author(s):  
William R Rice
Keyword(s):  
Y Chromosome ◽  
Alternative Model ◽  
Sex Chromosome ◽  
Deleterious Mutations ◽  
Genetic Hitchhiking ◽  
New Model ◽  
Muller's Ratchet ◽  
Genetic Activity ◽  
Muller’S Ratchet ◽  
Selection For

ABSTRACT A new model for the evolution of reduced genetic activity of the Y sex chromosome is described. The model is based on the process of genetic hitchhiking. It is shown that the Y chromosome can gradually lose its genetic activity due to the fixation of deleterious mutations that are linked with other beneficial genes. Fixation of deleterious Y-linked mutations generates locus-specific selection for dosage tolerance and/or compensation. The hitchhiking effect is most pronounced when operating in combination with an alternative model, Muller's ratchet. It is shown, however, that the genetic hitchhiking mechanism can operate under conditions where Muller's ratchet is ineffective.

scholarly journals Does Muller's ratchet work with selfing?

1978 ◽  
Vol 32 (3) ◽  
pp. 289-293 ◽  
Author(s):  
R. Heller ◽  
J. Maynard Smith
Keyword(s):  
Large Class ◽  
Deleterious Mutations ◽  
Asexual Population ◽  
Muller's Ratchet ◽  
Slightly Deleterious Mutations ◽  
Muller’S Ratchet

SUMMARYThe accumulation of deleterious mutations in a finite diploid selfing population is investigated. It is shown that the conditions for accumulation are very similar to those for the accumulation of mutations in an asexual population by ‘Muller's ratchet’. The ratchet is likely to operate in both types of population if there is a large class of slightly deleterious mutations.

scholarly journals Muller's ratchet, epistasis and mutation effects.

Genetics ◽  
1995 ◽  
Vol 141 (1) ◽  
pp. 431-437 ◽  
Author(s):  
D Butcher
Keyword(s):  
Deleterious Mutation ◽  
Strong Dependence ◽  
Continuous Distribution ◽  
Growth Parameter ◽  
Gene Interaction ◽  
Reproductive Age ◽  
Asexual Population ◽  
Muller's Ratchet ◽  
Muller’S Ratchet ◽  
Mutation Distribution

Abstract In this study, computer simulation is used to show that despite synergistic epistasis for fitness, Muller's ratchet can lead to lethal fitness loss in a population of asexuals through the accumulation of deleterious mutations. This result contradicts previous work that indicated that epistasis will halt the ratchet. The present results show that epistasis will not halt the ratchet provided that rather than a single deleterious mutation effect, there is a distribution of deleterious mutation effects with sufficient density near zero. In addition to epistasis and mutation distribution, the ability of Muller's ratchet to lead to the extinction of an asexual population under epistasis for fitness depends strongly on the expected number of offspring that survive to reproductive age. This strong dependence is not present in the nonepistatic model and suggests that interpreting the population growth parameter as fecundity is inadequate. Because a continuous distribution of mutation effects is used in this model, an emphasis is placed on the dynamics of the mutation effect distribution rather than on the dynamics of the number of least mutation loaded individuals. This perspective suggests that current models of gene interaction are too simple to apply directly to long-term prediction for populations undergoing the ratchet.

scholarly journals Muller's Ratchet and the Pattern of Variation at a Neutral Locus

Genetics ◽  
2002 ◽  
Vol 161 (2) ◽  
pp. 835-848 ◽  
Author(s):  
Isabel Gordo ◽  
Arcadio Navarro ◽  
Brian Charlesworth
Keyword(s):  
Genetic Diversity ◽  
Rare Variants ◽  
Deleterious Mutations ◽  
Asexual Population ◽  
Muller's Ratchet ◽  
Neutral Locus ◽  
Muller’S Ratchet ◽  
Considerable Distortion ◽  
Pattern Of Variation ◽  
Analytical Expressions

Abstract The levels and patterns of variation at a neutral locus are analyzed in a haploid asexual population undergoing accumulation of deleterious mutations due to Muller's ratchet. We find that the movement of Muller's ratchet can be associated with a considerable reduction in genetic diversity below classical neutral expectation. The extent to which variability is reduced is a function of the deleterious mutation rate, the fitness effects of the mutations, and the population size. Approximate analytical expressions for the expected genetic diversity are compared with simulation results under two different models of deleterious mutations: a model where all deleterious mutations have equal effects and a model where there are two classes of deleterious mutations. We also find that Muller's ratchet can produce a considerable distortion in the neutral frequency spectrum toward an excess of rare variants.

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.

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