scholarly journals Why Chromosome Palindromes?

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Esther Betrán ◽  
Jeffery P. Demuth ◽  
Anna Williford
Keyword(s):  
Gene Conversion ◽  
Y Chromosome ◽  
Adaptive Evolution ◽  
Purifying Selection ◽  
Duplicate Gene ◽  
Adaptive Significance ◽  
Deleterious Mutations ◽  
Initial Fixation ◽  
Selection For ◽  
Y Degeneration

We look at sex-limited chromosome (Y or W) evolution with particular emphasis on the importance of palindromes. Y chromosome palindromes consist of inverted duplicates that allow for local recombination in an otherwise nonrecombining chromosome. Since palindromes enable intrachromosomal gene conversion that can help eliminate deleterious mutations, they are often highlighted as mechanisms to protect against Y degeneration. However, the adaptive significance of recombination resides in its ability to decouple the evolutionary fates of linked mutations, leading to both a decrease in degeneration rate and an increase in adaptation rate. Our paper emphasizes the latter, that palindromes may exist to accelerate adaptation by increasing the potential targets and fixation rates of incoming beneficial mutations. This hypothesis helps reconcile two enigmatic features of the “palindromes as protectors” view: (1) genes that are not located in palindromes have been retained under purifying selection for tens of millions of years, and (2) under models that only consider deleterious mutations, gene conversion benefits duplicate gene maintenance but not initial fixation. We conclude by looking at ways to test the hypothesis that palindromes enhance the rate of adaptive evolution of Y-linked genes and whether this effect can be extended to palindromes on other chromosomes.

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.

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 GroEL/S helps purge deleterious mutations and reduce genetic diversity during adaptive protein evolution

2021 ◽  
Author(s):  
Bharat Ravi Iyengar ◽  
Andreas Wagner
Keyword(s):  
Genetic Diversity ◽  
Adaptive Evolution ◽  
High Throughput Sequencing ◽  
Evolutionary Dynamics ◽  
Stabilizing Selection ◽  
List Type ◽  
Deleterious Mutations ◽  
Client Proteins ◽  
Selection For ◽  
Evolving Populations

AbstractChaperones are proteins that help other proteins fold. They also affect the adaptive evolution of their client proteins by buffering deleterious mutations and increasing the genetic diversity of evolving proteins. We study how the bacterial chaperone GroE (GroEL + GroES) affects the evolution of green fluorescent protein (GFP). To this end we subjected GFP to multiple rounds of mutation and selection for its color phenotype in four replicate E. coli populations, and studied its evolutionary dynamics through high-throughput sequencing and mutant engineering. We evolved GFP both under stabilizing selection for its ancestral (green) phenotype, and to directional selection for a new (cyan) phenotype,. We did so both under low and high expression of the chaperone GroE. In contrast to prevailing wisdom, we observe that GroE does not just buffer but also helps purge deleterious mutations from evolving populations. In doing so, GroE helps reduce the genetic diversity of evolving populations. In addition, it causes phenotypic heterogeneity in mutants with the same genotype, potentiating their effect in some cells, and buffering it in others. Our observations show that chaperones can affect adaptive evolution through more than one mechanism.HighlightsGroE reduces genetic diversityGroE potentiates the effect of deleterious mutationsGroE intensifies purifying selection and leads to higher activity of client proteins

scholarly journals Site level factors that affect the rate of adaptive evolution in humans and chimpanzees; the effect of contracting population size.

2021 ◽  
Author(s):  
Vivak Soni ◽  
Ana Filipa Moutinho ◽  
Adam Eyre-Walker
Keyword(s):  
Amino Acids ◽  
Protein Structure ◽  
Amino Acid ◽  
Population Size ◽  
Adaptive Evolution ◽  
Purifying Selection ◽  
Selective Constraint ◽  
Drosophila Species ◽  
Deleterious Mutations ◽  
The Mean

It has previously been shown in other species that the rate of adaptive evolution is higher at sites that are more exposed in a protein structure and lower between amino acid pairs that are more dissimilar. We have investigated whether these patterns are found in the divergence between humans and chimpanzees using an extension of the MacDonald-Kreitman test. We confirm previous findings and find that the rate of adaptive evolution, relative to the rate of mutation, is higher for more exposed amino acids, lower for amino acid pairs that are more dissimilar in terms of their polarity, volume and lower for amino acid pairs that are subject to stronger purifying selection, as measured by the ratio of the numbers of non-synonymous to synonymous polymorphisms (pN/pS). However, the slope of this latter relationship is significantly shallower than in Drosophila species. We suggest that this is due to the population contraction that has occurred since humans and chimpanzees diverged. We demonstrate theoretically that population size reduction can generate an artefactual positive correlation between the rate of adaptive evolution and any factor that is correlated to the mean strength of selection acting against deleterious mutations, even if there has been no adaptive evolution (the converse is also expected). Our measure of selective constraint, pN/pS, is negatively correlated to the mean strength of selection, and hence we would expect the correlation between the rate of adaptive evolution to also be negatively correlated to pN/pS, if there is no adaptive evolution. The fact that our rate of adaptive evolution is positively correlated to pN/pS suggests that the correlation does genuinely exist, but that is has been attenuated by population size contraction.

The Age of Nonsynonymous and Synonymous Mutations in Animal mtDNA and Implications for the Mildly Deleterious Theory

Genetics ◽  
1999 ◽  
Vol 153 (1) ◽  
pp. 497-506 ◽  
Author(s):  
Rasmus Nielsen ◽  
Daniel M Weinreich
Keyword(s):  
Dna Sequences ◽  
Purifying Selection ◽  
Data Sets ◽  
Deleterious Mutations ◽  
Synonymous Mutations ◽  
Weak Evidence ◽  
Mitochondrial Data ◽  
The Mean ◽  
Excess Number ◽  
Neutral Mutations

Abstract McDonald/Kreitman tests performed on animal mtDNA consistently reveal significant deviations from strict neutrality in the direction of an excess number of polymorphic nonsynonymous sites, which is consistent with purifying selection acting on nonsynonymous sites. We show that under models of recurrent neutral and deleterious mutations, the mean age of segregating neutral mutations is greater than the mean age of segregating selected mutations, even in the absence of recombination. We develop a test of the hypothesis that the mean age of segregating synonymous mutations equals the mean age of segregating nonsynonymous mutations in a sample of DNA sequences. The power of this age-of-mutation test and the power of the McDonald/Kreitman test are explored by computer simulations. We apply the new test to 25 previously published mitochondrial data sets and find weak evidence for selection against nonsynonymous mutations.

scholarly journals Experiments on the role of deleterious mutations as stepping stones in adaptive evolution

2013 ◽  
Vol 110 (34) ◽  
pp. E3171-E3178 ◽  
Author(s):  
Arthur W. Covert ◽  
Richard E. Lenski ◽  
Claus O. Wilke ◽  
Charles Ofria
Keyword(s):  
Adaptive Evolution ◽  
Deleterious Mutations ◽  
Stepping Stones

scholarly journals Gene conversion and purifying selection of a placenta-specific ERV-V envelope gene during simian evolution

2008 ◽  
Vol 8 (1) ◽  
pp. 266 ◽  
Author(s):  
Anders L Kjeldbjerg ◽  
Palle Villesen ◽  
Lars Aagaard ◽  
Finn Skou Pedersen
Keyword(s):  
Gene Conversion ◽  
Purifying Selection ◽  
Envelope Gene ◽  
Selection Of

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 Interlocus gene conversion events introduce deleterious mutations into at least 1% of human genes associated with inherited disease

2011 ◽  
Vol 22 (3) ◽  
pp. 429-435 ◽  
Author(s):  
C. Casola ◽  
U. Zekonyte ◽  
A. D. Phillips ◽  
D. N. Cooper ◽  
M. W. Hahn
Keyword(s):  
Gene Conversion ◽  
Deleterious Mutations ◽  
Inherited Disease ◽  
Human Genes
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