title: Short- and long-term benefits and detriments to recombination under antagonistic coevolution.
abstract: We explored the evolution of recombination under antagonistic coevolution, concentrating on the equilibrium frequencies of modifier alleles causing recombination in initially nonrecombining populations. We found that the equilibrium level of recombination in the host depended not only on parasite virulence, but also on the strength of the modifier allele, and on whether or not the modifier was physically linked to the parasite interaction loci. Nonetheless, the maximum level of recombination for linked loci at equilibrium was about 0.3 (60% of free recombination) for interactions with highly virulent parasites; the level decreased for unlinked modifiers, and for lower levels of parasite virulence. We conclude that recombination spreads because it provides a combination of an immediate (next-generation) fitness benefit and a delayed (two or more generations) increase in the rate of response to directional selection. The relative impact of these two mechanisms depends on the virulence of parasites early in the spread of the modifier, but a trade-off between the two dictates the equilibrium modifier frequency for all nonzero virulences that we examined. In addition, population mean fitness was higher in populations at intermediate equilibria than populations fixed for free recombination or no recombination. The difference, however, was not enough on its own to overcome the two-fold cost of producing males.
authors.affiliation: Department of Zoology, University of British Columbia, Vancouver, BC, Canada and Department of Zoology, University of Wisconsin-Madison, Madison, WI 53706, USA.
authors.forename: A D
authors.initials: AD
authors.lastname: Peters
authors.forename: C M
authors.initials: CM
authors.lastname: Lively
mesh_terms: D000483:Alleles; D000818:Animals; D019143:Evolution, Molecular; D008040:Genetic Linkage; D006790:Host-Parasite Interactions; D008957:Models, Genetic; D011995:Recombination, Genetic; D012641:Selection, Genetic; D014774:Virulence