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Modifier Allele (modifier + allele)
Selected AbstractsDO WOLBACHIA- ASSOCIATED INCOMPATIBILITIES PROMOTE POLYANDRY?EVOLUTION, Issue 1 2008Fleur E. Champion de Crespigny The genetic incompatibility avoidance hypothesis as an explanation for the polyandrous mating strategies (mating with more than one male) of females of many species has received significant attention in recent years. It has received support from both empirical studies and a meta-analysis, which concludes that polyandrous females enjoy increased reproductive success through improved offspring viability relative to monandrous females. In this study we investigate whether polyandrous female Drosophila simulans improve their fitness relative to monandrous females in the face of severe Wolbachia- associated reproductive incompatibilities. We use the results of this study to develop models that test the predictions that Wolbachia should promote polyandry, and that polyandry itself may constrain the spread of Wolbachia. Uniquely, our models allow biologically relevant rates of incompatibility to coevolve with a polyandry modifier allele, which allows us to evaluate the fate of the modifier and that of Wolbachia. Our empirical results reveal that polyandrous females significantly reduce the reproductive costs of Wolbachia, owing to infected males being poor sperm competitors. The models show that this disadvantage in sperm competition can inhibit or prevent the invasion of Wolbachia. However, despite the increased reproductive success obtained by polyandrous females, the spread of a polyandry modifier allele is constrained by any costs that might be associated with polyandry and the low frequency of incompatible matings when Wolbachia has reached a stable equilibrium. Therefore, although incompatibility avoidance may be a benefit of polyandry, our findings do not support the hypothesis that genetic incompatibilities caused by Wolbachia promote the evolution of polyandry. [source] THE EVOLUTION OF GENETIC CANALIZATION UNDER FLUCTUATING SELECTIONEVOLUTION, Issue 1 2000Tadeusz J. Kawecki Abstract., If the direction of selection changes from generation to generation, the ability to respond to selection is maladaptive: the response to selection in one generation leads to reduced fitness in the next. Because the response is determined by the amount of genetic variance expressed at the phenotypic level, rapidly fluctuating selection should favor modifier genes that reduce the phenotypic effect of alleles segregating at structural loci underlying the trait. Such reduction in phenotypic expression of genetic variation has been named "genetic canalization." I support this argument with a series of two- and multilocus models with alternating linear selection and Gaussian selection with fluctuating optimum. A canalizing modifier gene affects the fitness of its carriers in three ways: (1) it reduces the phenotypic consequences of genetic response to previous selection; (2) it reduces the genetic response to selection, which is manifested as linkage disequilibrium between the modifier and structural loci; and (3) it reduces the phenotypic variance. The first two effects reduce fitness under directional selection sustained for several generations, but improve fitness when the direction of selection has just been reversed. The net effect tends to favor a canalizing modifier under rapidly fluctuating selection regimes (period of eight generations or less). The third effect improves fitness of the modifier allele if the fitness function is convex and reduces it if the function is concave. Under fluctuating Gaussian selection, the population is more likely to experience the concave portion of the fitness function when selection is stronger. Therefore, only weak to moderately strong fluctuating Gaussian selection favors genetic canalization. This paper considerably broadens the conditions that favor genetic canalization, which so far has only been postulated to evolve under long-term stabilizing selection. [source] Short- and long-term benefits and detriments to recombination under antagonistic coevolutionJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 3 2007A. D. PETERS 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. [source] | ||||||||||