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.

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.

The degenerate Y chromosome – can conversion save it?

2004 ◽  
Vol 16 (5) ◽  
pp. 527 ◽  
Author(s):  
Jennifer A. Marshall Graves
Keyword(s):  
Gene Conversion ◽  
Y Chromosome ◽  
Genetic Drift ◽  
Sex Chromosome ◽  
Chromosome Differentiation ◽  
Y Chromosomes ◽  
Speed Up ◽  
Selection For ◽  
Human Y Chromosome

The human Y chromosome is running out of time. In the last 300 million years, it has lost 1393 of its original 1438 genes, and at this rate it will lose the last 45 in a mere 10 million years. But there has been a proposal that perhaps rescue is at hand in the form of recently discovered gene conversion within palindromes. However, I argue here that although conversion will increase the frequency of variation of the Y (particularly amplification) between Y chromosomes in a population, it will not lead to a drive towards a more functional Y. The forces of evolution have made the Y a genetically isolated, non-recombining entity, vulnerable to genetic drift and selection for favourable new variants sharing the Y with damaging mutations. Perhaps it will even speed up the decline of the Y chromosome and the onset of a new round of sex-chromosome differentiation. The struggle to preserve males may perhaps lead to hominid speciation.

Muller's Ratchet and the evolution of supernumerary chromosomes

Genome ◽  
1990 ◽  
Vol 33 (6) ◽  
pp. 818-824 ◽  
Author(s):  
David M. Green
Keyword(s):  
Genetic Information ◽  
Sex Chromosome ◽  
Chromosome Complement ◽  
Evolutionary Constraint ◽  
Supernumerary Chromosomes ◽  
Muller's Ratchet ◽  
Heteromorphic Sex Chromosomes ◽  
Muller’S Ratchet ◽  
Over Time ◽  
Chromosome Heteromorphism

Supernumerary chromosomes arise from portions of the normal chromosome complement through nondisjunction, fragmentation, or other mechanisms. Once present in the genome, they are subject to virtually the same genetic conditions that affect the evolutionary degeneration of heteromorphic sex chromosomes. Y or W chromosomes occur only in the presence of X or Z chromosomes, respectively, just as supernumeraries never occur except in the presence of the complete regular karyotype containing their progenitor sequences. Thus, mechanisms that can account for the evolution of sex-chromosome heteromorphism can also be invoked to explain the degeneration process of supernumerary chromosomes after their origination. Incipient supernumeraries initially have genes identical with those on progenitor chromosomes. This frees them from the evolutionary constraint of carrying nonduplicated genetic information, just as in Y and W chromosomes during early stages of sex-chromosome differentiation. The degeneration of supernumerary chromosomes may thus proceed via the mechanism of Muller's Ratchet. This hypothesis predicts that supernumerary chromosomes should lose functional loci, lose sequence homology with the regular genome, and gain heterochromatin over time, resulting in multiple heteromorphic forms of degenerate supernumeraries within and between populations, as is commonly observed.Key words: supernumerary chromosomes, B chromosomes, evolution, origin, Muller's Ratchet.

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.

The nature of gene evolution on the mammalian Y chromosome: lessons from Sry

1995 ◽  
Vol 350 (1333) ◽  
pp. 221-227 ◽  
Keyword(s):  
Molecular Evolution ◽  
Y Chromosome ◽  
Gene Evolution ◽  
Small Region ◽  
Male Meiosis ◽  
Effective Population ◽  
Muller's Ratchet ◽  
Amino Acid Divergence ◽  
Muller’S Ratchet ◽  
The Hill

With the exception of a small region, heteromorphic sex chromosomes of mammals do not undergo recombination in male meiosis. As a result, the majority of the Y chromosome is clonally transmitted through paternal lineages. Numerous phenomena, including the Hill-Robertson effect, Muller’s ratchet, genetic hitch-hiking, and male-driven molecular evolution, are associated with the special transmission properties of the Y chromosome, and can potentially explain the tempo and pattern of gene evolution on the mammalian Y. We explore these phenomena in light of comparative data from the Y-linked sex-determining locus, Sry . Sry exhibits rapid amino acid divergence between species and little to no variation within species. We find no evidence for directional selection acting on this locus. The pattern of evolution between species is consistent with the Hill-Robertson effect and Muller’s ratchet. Lack of variation in Sry within species may reflect genetic hitch-hiking, however, we cannot exclude the confounding effects of small effective population size of Y chromosomes. We find no support for male-driven molecular evolution for Sry in Old World mice and rats. However, a more appropriate test of this hypothesis would be to compare the evolution of Sry to the X-linked Sox3 gene in these same species. Clearly, more comparative studies of Sry and other Y-linked loci are needed to characterize the effects of Y chromosome transmission on the evolution of Y-linked sequences.

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 Integrating ecology and evolution to study hypothetical dynamics of algal blooms and Muller’s ratchet using Evolvix

2017 ◽  
Author(s):  
Sarah Northey ◽  
Courtney Hove ◽  
Justine Kao ◽  
Jon Ide ◽  
Janel McKinney ◽  
...  
Keyword(s):  
Dna Repair ◽  
Nutrient Availability ◽  
Continuous Time ◽  
Algal Blooms ◽  
Predation Pressure ◽  
Mutation Rates ◽  
Deleterious Mutations ◽  
Muller's Ratchet ◽  
Slightly Deleterious Mutations ◽  
Muller’S Ratchet

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.

scholarly journals Integrating ecology and evolution to study hypothetical dynamics of algal blooms and Muller’s ratchet using Evolvix

2017 ◽  
Author(s):  
Sarah Northey ◽  
Courtney Hove ◽  
Justine Kao ◽  
Jon Ide ◽  
Janel McKinney ◽  
...  
Keyword(s):  
Dna Repair ◽  
Nutrient Availability ◽  
Continuous Time ◽  
Algal Blooms ◽  
Predation Pressure ◽  
Mutation Rates ◽  
Deleterious Mutations ◽  
Muller's Ratchet ◽  
Slightly Deleterious Mutations ◽  
Muller’S Ratchet

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.

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.

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