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

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.

1978 ◽  
Vol 32 (3) ◽  
pp. 289-293 ◽  
Author(s):  
R. Heller ◽  
J. Maynard Smith

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.


1993 ◽  
Vol 61 (3) ◽  
pp. 225-231 ◽  
Author(s):  
Wolfgang Stephan ◽  
Lin Chao ◽  
Joanne Guna Smale

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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Xin Zhao ◽  
Zhi Li ◽  
Miao Ding ◽  
Tao Wang ◽  
Ming-Tao Wang ◽  
...  

Unisexual lineages are commonly considered to be short-lived in the evolutionary process as accumulation of deleterious mutations stated by Muller’s ratchet. However, the gynogenetic hexaploid gibel carp (Carassius gibelio) with existence over 0.5 million years has wider ecological distribution and higher genetic diversity than its sexual progenitors, which provides an ideal model to investigate the underlying mechanisms on countering Muller’s ratchet in unisexual taxa. Unlike other unisexual lineages, the wild populations of gibel carp contain rare and variable proportions of males (1–26%), which are determined via two strategies including genotypic sex determination and temperature-dependent sex determination. Here, we used a maternal gibel carp from strain F to be mated with a genotypic male from strain A+, a temperature-dependent male from strain A+, and a male from another species common carp (Cyprinus carpio), respectively. When the maternal individual was mated with the genotypic male, a variant of gynogenesis was initiated, along with male occurrence, accumulation of microchromosomes, and creation of genetic diversity in the offspring. When the maternal individual was mated with the temperature-dependent male and common carp, typical gynogenesis was initiated that all the offspring showed the same genetic information as the maternal individual. Subsequently, we found out that the genotypic male nucleus swelled and contacted with the female nucleus after fertilization although it was extruded from the female nucleus eventually, which might be associated with the genetic variation in the offspring. These results reveal that genotypic males play an important role in the creation of genetic diversity in gynogenetic gibel carp, which provides insights into the evolution of unisexual reproduction.


1997 ◽  
Vol 70 (1) ◽  
pp. 63-73 ◽  
Author(s):  
BRIAN CHARLESWORTH ◽  
DEBORAH CHARLESWORTH

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.


Genetics ◽  
1994 ◽  
Vol 136 (4) ◽  
pp. 1469-1473 ◽  
Author(s):  
A S Kondrashov

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.


Genetics ◽  
1987 ◽  
Vol 116 (1) ◽  
pp. 161-167
Author(s):  
William R Rice

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.


2018 ◽  
Author(s):  
Logan Chipkin ◽  
Peter Olofsson ◽  
Ryan C. Daileda ◽  
Ricardo B. R. Azevedo

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.


2017 ◽  
Author(s):  
Sarah Northey ◽  
Courtney Hove ◽  
Justine Kao ◽  
Jon Ide ◽  
Janel McKinney ◽  
...  

Algal blooms have been the subject of considerable research as they occur over various spatial and temporal scales and can produce toxins that disrupt their ecosystem. Algal blooms are often governed by nutrient availability however other limitations exist. Algae are primary producers and therefore subject to predation which can keep populations below levels supported by nutrient availability. If algae as prey mutate to gain the ability to produce toxins deterring predators, they may increase their survival rates and form blooms unless other factors counter their effective increase in growth rate. Where might such mutations come from? Clearly, large populations of algae will repeatedly experience mutations knocking-out DNA repair genes, increasing mutation rates, and with them the chance of acquiring de-novo mutations producing a toxin against predators. We investigate this hypothetical scenario by simulation in the Evolvix modeling language. We modeled a sequence of steps that in principle can allow a typical asexual algal population to escape predation pressure and form a bloom with the help of mutators. We then turn our attention to the unavoidable side effect of generally increased mutation rates, many slightly deleterious mutations. If these accumulate at sufficient speed, their combined impact on fitness might place upper limits on the duration of algal blooms. These steps are required: (1) Random mutations result in the loss of DNA repair mechanisms. (2) Increased mutation rates make it more likely to acquire the ability to produce toxins by altering metabolism. (3) Toxins deter predators providing algae with growth advantages that can mask linked slightly deleterious mutational effects. (4) Reduced predation pressure enables blooms if algae have sufficient nutrients. (5) Lack of recombination results in the accumulation of slightly deleterious mutations as predicted by Muller’s ratchet. (6) If fast enough, deleterious mutation accumulation eventually leads to mutational meltdown of toxic blooming algae. (7) Non-mutator algal populations are not affected due to ongoing predation pressure. Our simulation models integrate ecological continuous-time dynamics of predator-prey systems with the population genetics of a simplified Muller’s ratchet model using Evolvix. Evolvix maps these models to Continuous-Time Markov Chain models that can be simulated deterministically or stochastically depending on the question. The current model is incomplete; we plan to investigate many parameter combinations to produce a more robust model ensemble with stable links to reasonable parameter estimates. However, our model already has several intriguing features that may allow for the eventual development of observation methods for monitoring ecosystem health. Our work also highlights a growing need to simulate integrated models combining ecological processes, multi-level population dynamics, and evolutionary genetics in a single computational run.


2017 ◽  
Author(s):  
Sarah Northey ◽  
Courtney Hove ◽  
Justine Kao ◽  
Jon Ide ◽  
Janel McKinney ◽  
...  

Algal blooms have been the subject of considerable research as they occur over various spatial and temporal scales and can produce toxins that disrupt their ecosystem. Algal blooms are often governed by nutrient availability however other limitations exist. Algae are primary producers and therefore subject to predation which can keep populations below levels supported by nutrient availability. If algae as prey mutate to gain the ability to produce toxins deterring predators, they may increase their survival rates and form blooms unless other factors counter their effective increase in growth rate. Where might such mutations come from? Clearly, large populations of algae will repeatedly experience mutations knocking-out DNA repair genes, increasing mutation rates, and with them the chance of acquiring de-novo mutations producing a toxin against predators. We investigate this hypothetical scenario by simulation in the Evolvix modeling language. We modeled a sequence of steps that in principle can allow a typical asexual algal population to escape predation pressure and form a bloom with the help of mutators. We then turn our attention to the unavoidable side effect of generally increased mutation rates, many slightly deleterious mutations. If these accumulate at sufficient speed, their combined impact on fitness might place upper limits on the duration of algal blooms. These steps are required: (1) Random mutations result in the loss of DNA repair mechanisms. (2) Increased mutation rates make it more likely to acquire the ability to produce toxins by altering metabolism. (3) Toxins deter predators providing algae with growth advantages that can mask linked slightly deleterious mutational effects. (4) Reduced predation pressure enables blooms if algae have sufficient nutrients. (5) Lack of recombination results in the accumulation of slightly deleterious mutations as predicted by Muller’s ratchet. (6) If fast enough, deleterious mutation accumulation eventually leads to mutational meltdown of toxic blooming algae. (7) Non-mutator algal populations are not affected due to ongoing predation pressure. Our simulation models integrate ecological continuous-time dynamics of predator-prey systems with the population genetics of a simplified Muller’s ratchet model using Evolvix. Evolvix maps these models to Continuous-Time Markov Chain models that can be simulated deterministically or stochastically depending on the question. The current model is incomplete; we plan to investigate many parameter combinations to produce a more robust model ensemble with stable links to reasonable parameter estimates. However, our model already has several intriguing features that may allow for the eventual development of observation methods for monitoring ecosystem health. Our work also highlights a growing need to simulate integrated models combining ecological processes, multi-level population dynamics, and evolutionary genetics in a single computational run.


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