The first steps of animal speciation are thought to be the development of sexual isolating mechanisms. In contrast to recent progress in understanding the genetic basis of postzygotic isolating mechanisms, little is known about the genetic architecture of sexual isolation. Here, we have subjected Drosophila melanogaster to 29 generations of replicated divergent artificial selection for mating speed. The phenotypic response to selection was highly asymmetrical in the direction of reduced mating speed, with estimates of realized heritability averaging 7%. The selection response was largely attributable to a reduction in female receptivity. We assessed the whole genome transcriptional response to selection for mating speed using Affymetrix GeneChips and a rigorous statistical analysis. Remarkably, >3,700 probe sets (21% of the array elements) exhibited a divergence in message levels between the Fast and Slow replicate lines. Genes with altered transcriptional abundance in response to selection fell into many different biological process and molecular function Gene Ontology categories, indicating substantial pleiotropy for this complex behavior. Future functional studies are necessary to test the extent to which transcript profiling of divergent selection lines accurately predicts genes that directly affect the selected trait.Species are groups of actually or potentially interbreeding natural populations, which are reproductively isolated from other such groups.Recent studies by the students of animal behavior, as well as the revised interpretation of many earlier observations, indicate that behavior differences are among animals the most important factor in restricting random mating between closely related forms.E. Mayr, 1942
The genomic rate and distribution of effects of deleterious mutations are important parameters in evolutionary theory. The most detailed information comes from the work of Mukai and Ohnishi, who allowed mutations to accumulate on Drosophila melanogaster second chromosomes, shielded from selection and recombination by being maintained heterozygous in males. Averaged over studies, the estimated rate of nonlethal viability mutations per second chromosome per generation under an equal-effects model, U BM , was 0.12, suggesting a high genomic mutation rate. We have performed a mutation-accumulation experiment similar to those of Mukai and Ohnishi, except that three large homozygous control populations were maintained. Egg-toadult viability of 72 nonlethal mutation-accumulation (MA) lines and the controls was assayed after 27-33 generations of mutation accumulation. The rate of decline in mean viability was significantly lower than observed by Mukai, and the rate of increase in among-line variance was significantly higher. Our U BM estimate of 0.02 is much lower than the previous estimates. Our results suggest that the rate of mutations that detectably reduce viability may not be much greater than the lethal mutation rate (0.01 in these lines), but the results also are consistent with models that include many mutations with very small effects.The genomic rate and distribution of effects of deleterious mutations are critical parameters in models of the evolution of sex and recombination (1, 2), of the long-term viability of small populations (3, 4), and of molecular and phenotypic variation (5, 6). The classic experiments of Mukai (7,8) and Ohnishi (9) on Drosophila melanogaster, in which mutations were allowed to accumulate on chromosomes shielded from selection and recombination, gave evidence that the rate of mutations with mild negative effects (Ͻ10%) on pre-adult viability is on the order of one per zygote per generation. Among other important consequences, such a high rate of mildly deleterious mutations could doom populations with effective sizes of a few hundred to extinction (3, 10).More recent work, however, has given reason to question whether rates of mutations with detectable effects on fitness traits are typically as high as estimated by Mukai and Ohnishi. Experiments on Drosophila (11) and Caenorhabditis elegans (12) showed much slower declines in fitness traits on relaxation of selection against new mutations than observed by Mukai and Ohnishi. Although methodological differences could explain this discrepancy (13), another possibility is that the mean decline was overestimated in the earlier studies. This could have happened because the studies lacked concurrent controls for viability changes in the mutation-accumulation (MA) lines; viability instead was compared with base generation values that were obtained months earlier. If some change in experimental conditions occurred in the interim that depressed actual or apparent viability, both the mean decline and the genomic mutation rate would hav...
Many studies have documented the existence of genotype-environment interaction (GEI) for traits closely related to fitness in natural populations. A type of GEI that is commonly observed is changes in the fitness ranking of genetic groups (families, clones, or inbred lines) in different environments. We refer to such changes in ranking as crossing of reaction norms for fitness. A common interpretation of crossing of reaction norms for fitness is that selection favors different alleles in the different environments (i.e., that "trade-offs" exist). If this is the case, selection could maintain genetic variation, and even lead to reproductive isolation between subpopulations using different environments. Even if the same alleles are favored in every environment, however, deleterious mutations that vary in the magnitude of their effect depending on environment could cause reaction norms for fitness to cross. If deleterious mutations with environment-dependent effects are responsible for maintaining much of the variation leading to crossing of reaction norms for fitness in natural populations, it should be possible to observe crossing of reaction norms for fitness among otherwise genetically identical lines bearing newly arisen spontaneous mutations. We examined the contribution of new mutations to GEI for fitness in Drosophila melanogaster. Eighteen lines were derived from a common, highly inbred base stock, and maintained at a population size of 10 pairs for over 200 generations, to allow them to accumulate spontaneous mutations. Because of the small population size of the lines, selection against mildly deleterious mutations should have been relatively ineffective. The lines were tested for productivity (number of surviving adult progeny from a standard number of parents) in five different environmental treatments, comprising different food media, temperatures, and levels of competition. The lines showed highly significant GEI for productivity, owing largely to considerable changes in ranking in the different environments. We conclude that mutations that are deleterious on average, but whose quantitative effects depend on environment, could be responsible for maintaining much of the variation leading to crossing of reaction norms for fitness that has been observed in samples of D. melanogaster from the wild.
The genomic rate of mildly deleterious mutations (U) figures prominently in much evolutionary and ecological theory. In Drosophila melanogaster, estimates of U have varied widely, from <0.1 to nearly 1 per zygote. The source of this variation is unknown, but could include differences in the conditions used for assaying fitness traits. We examined how assay conditions affect estimates of the rates and effects of viability-depressing mutations in two sets of lines with accumulated spontaneous mutations on the second chromosome. In each set, the among-line variance in egg-to-adult viability was significantly greater when viability was assayed using a high parental density than when it was assayed using a low density. In contrast, the proportional decline in viability due to new mutations did not differ between densities. Two other manipulations, lowering the temperature and adding ethanol to the medium, had no significant effects on either the mean decline or among-line variance. Cross-environment genetic correlations in viability were generally close to one, implying that most mutations reduced viability in all environments. Using data from the low-density, lower-bound estimates of U approached the classic, high values of Mukai and Ohnishi; at the high density, U estimates were similar to recently reported low values. The difference in estimated mutation rates, taken at face value, would imply that many mutations affected fitness at low density but not at high density, but this is shown to be incompatible with the observed high cross-environment correlations. Possible reasons for this discrepancy are discussed. Regardless of the interpretation, the results show that assay conditions can have a large effect on estimates of mutational parameters for fitness traits.
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