PubMed · 6755261
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T Petes, G R Fink. 1982-11-18. Gene conversion between repeated genes.. https://doi.org/10.1038/300216a0
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GC-biased gene conversion (gBGC) is a widespread evolutionary force associated with meiotic recombination that favors the accumulation of deleterious AT to GC substitutions in proteins, moving them away from their fitness optimum. In many mammals, recombination hotspots have a rapid turnover, leading to episodic gBGC, with the accumulation of deleterious mutations stopping when the recombination hotspot dies. Selection is therefore expected to act to repair the damage caused by gBGC episodes through compensatory evolution. However, this process has never been studied or quantified so far. Here, we analyzed the nucleotide substitution pattern in coding sequences of a highly diversified group of Murinae rodents. Using phylogenetic analyses of about 70,000 coding exons, we identified numerous exon-specific, lineage-specific gBGC episodes, characterized by a clustering of synonymous AT to GC substitutions and by an increasing rate of nonsynonymous AT to GC substitutions, many of which are potentially deleterious. Analyzing the molecular evolution of the affected exons in downstream lineages, we found evidence for pervasive compensatory evolution after deleterious gBGC episodes. Compensation appears to occur rapidly after the end of the episode and to be driven by the standing genetic variation rather than new mutations. Our results demonstrate the impact of gBGC on the evolution of amino-acid sequences and underline the key role of epistasis in protein adaptation. This study contributes to a growing body of literature emphasizing that adaptive mutations, which arise in response to environmental changes, are just 1 subset of beneficial mutations, alongside mutations resulting from oscillations around the fitness optimum.
Of the 645 Japanese subjects studied, we have identified 10 individuals heterozygous for a chromosome with the triplicated alpha-globin loci. The frequency of the triple alpha-loci was 0.008 in this population, while that of the single alpha-locus, i.e., alpha-thalassemia 2 gene, might be lower than 0.0008. Analysis of haplotypes using particular RsaI site polymorphism in the alpha-globin gene complex strongly suggests that the triple alpha loci may have had multiple origins in this population.
A new mathematical approach to the description of interaction data (Ager and Haynes, 1987) is applied here to the interaction between heat and ultraviolet light (UV) in Saccharomyces cerevisiae. A strong synergism for cell killing is found to be associated with large increases in gene conversion (of up to 8-fold), and mutation (of up to 14-fold). Analysis of the interaction data for both wild-type and repair-deficient strains indicates that the heat-UV synergism arises via the inhibition of two different repair pathways. Unambiguous conclusions regarding the molecular mechanisms by which these repair processes are inhibited cannot be drawn on the basis of dose-response data alone. However, this approach does enable one to make well defined, empirical comparisons of the nature and kinetics of such interactions.