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Stress‐induced assortative mating and the evolution of stress resistance
Author(s) -
Winterer Juliette,
Weis Arthur E.
Publication year - 2004
Publication title -
ecology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.852
H-Index - 265
eISSN - 1461-0248
pISSN - 1461-023X
DOI - 10.1111/j.1461-0248.2004.00626.x
Subject(s) - assortative mating , biology , genetics , allele , resistance (ecology) , fixation (population genetics) , evolutionary biology , disruptive selection , mating , natural selection , phenotype , directional selection , genetic variation , selection (genetic algorithm) , ecology , gene , artificial intelligence , computer science
Abstract We show with a model that variation in environmental stress between generations facilitates the evolution of stress resistance through assortative mating. Stress induces delayed maturation of susceptible phenotypes, segregating their fertile period from resistant phenotypes. Assortment of mates enhances the responsiveness of populations to natural selection by inflating genetic variance. Thus, positive selection and inflated genetic variance in stressful environments can cause a strong evolutionary increase in resistance. By contrast, benign environments do not segregate phenotypes, and the random mating among phenotypes deflates genetic variance, leading to a weaker response to selection against resistance, assuming that resistance is costly. When environments vary randomly from benign to stressful, populations respond asymmetrically to negative and positive selection. This asymmetry (1) accelerates fixation of a resistance allele if resistance is generally favoured (stressful generations more frequent) but delays the loss of the allele if it is generally disfavoured (benign generations more frequent), and (2) it can push a resistance allele to fixation even when long‐term costs modestly exceed benefits. When resistance alleles pleiotropically delay mating, stress‐induced random mating has complementary effects. Serial autocorrelation in the stressor amplifies these effects. These results suggest a novel mechanism for the persistence of resistance polymorphisms.