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doi:10.1534/genetics.105.053108
A more recent version of this article appeared on June 1, 2006.
REGULAR RESEARCH PAPERS |
Effect of varying epistasis on the evolution of recombination
Roger D. Kouyos 1, Sarah P. Otto 2 and Sebastian Bonhoeffer 1*
1 ETH Zurich
2 University of British Columbia
* To whom correspondence should be addressed. E-mail: seb{at}env.ethz.ch.
Submitted on November 4, 2005
Revised on January 3, 2006
Accepted on 13 March 2006
Whether recombination decelerates or accelerates a population's response to selection depends, at least in part, on how fitness determining loci interact. Realistically, all genomes likely contain both fitness interactions with positive and with negative epistasis. Therefore, it is crucial to determine the conditions under which the potential beneficial effects of recombination with negative epistasis prevail over the detrimental effects of recombination with positive epistasis. Here, we examine the simultaneous effects of diverse epistatic interactions with different strengths and signs in a simplified model system with independent pairs of interacting loci and selection only acting on the haploid phase. We find that the average form of epistasis does not predict the average amount of linkage disequilibrium generated or the impact on a recombination modifier when compared to results using the entire distribution of epistatic effects and associated single mutant effects. Moreover, we show that epistatic interactions of a given strength can produce very different effects having the greatest impact when selection is weak. In summary, we observe that the evolution of recombination at mutation-selection balance might be driven by a small number of interactions with weak selection rather than by the average epistasis of all interactions. We illustrate this effect with an analysis of published data of Saccharomyces cerevisiae. Thus to draw conclusions on the evolution of recombination from experimental data, it is necessary to consider the distribution of epistatic interactions together with the associated selection coefficients.
Key Words: deleterious mutations, epistasis, modifier, population genetic model, recombination
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