Recombination Can Evolve in Large Finite Populations Given Selection on Sufficient Loci

It is well known that an allele causing increased recombination is expected to proliferate as a result of genetic drift in a finite population undergoing selection, without requiring other mechanisms. This is supported by recent simulations apparently demonstrating that, in small populations, drift...

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Published inGenetics (Austin) Vol. 165; no. 4; pp. 2249 - 2258
Main Authors Iles, Mark M, Walters, Kevin, Cannings, Chris
Format Journal Article
LanguageEnglish
Published United States Genetics Soc America 01.12.2003
Genetics Society of America
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Summary:It is well known that an allele causing increased recombination is expected to proliferate as a result of genetic drift in a finite population undergoing selection, without requiring other mechanisms. This is supported by recent simulations apparently demonstrating that, in small populations, drift is more important than epistasis in increasing recombination, with this effect disappearing in larger finite populations. However, recent experimental evidence finds a greater advantage for recombination in larger populations. These results are reconciled by demonstrating through simulation without epistasis that for m loci recombination has an appreciable selective advantage over a range of population sizes (am, bm). bm increases steadily with m while am remains fairly static. Thus, however large the finite population, if selection acts on sufficiently many loci, an allele that increases recombination is selected for. We show that as selection acts on our finite population, recombination increases the variance in expected log fitness, causing indirect selection on a recombination-modifying locus. This effect is enhanced in those populations with more loci because the variance in phenotypic fitnesses in relation to the possible range will be smaller. Thus fixation of a particular haplotype is less likely to occur, increasing the advantage of recombination.
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ISSN:0016-6731
1943-2631
1943-2631
DOI:10.1093/genetics/165.4.2249