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
Species often produce sterile hybrids early in their evolutionary divergence, and some evidence suggests that hybrid sterility may be associated with deviations or disruptions in gene expression. In support of this idea, many studies have shown that a high proportion of male-biased genes are underexpressed, compared with non-sex-biased genes, in sterile F 1 male hybrids of Drosophila species. In this study, we examined and compared patterns of misexpression in sterile F 1 male hybrids of Drosophila simulans and 2 of its sibling species, Drosophila mauritiana and Drosophila sechellia, at both the larval and adult life stages. We analyzed hybrids using both commercial Drosophila melanogaster microarrays and arrays we developed from reverse transcriptase-polymerase chain reactions of spermatogenesis and reproductionrelated transcripts from these species (sperm array). Although the majority of misexpressed transcripts were underexpressed, a disproportionate number of the overexpressed transcripts were located on the X chromosome. We detected a high overlap in the genes misexpressed between the 2 species pairs, and our sperm array was better at detecting such misexpression than the D. melanogaster array, suggesting possible weaknesses in the use of an array designed from another species. We found only minimal misexpression in the larval samples with the sperm array, suggesting that disruptions in spermatogenesis occur after this life stage. Further study of these misexpressed loci may allow us to identify precisely where disruptions in the spermatogenesis pathway occur.
Sexual isolating mechanisms that act before fertilization are often considered the most important genetic barriers leading to speciation in animals. While recent progress has been made toward understanding the genetic basis of the postzygotic isolating mechanisms of hybrid sterility and inviability, little is known about the genetic basis of prezygotic sexual isolation. Here, we map quantitative trait loci (QTL) contributing to prezygotic reproductive isolation between the sibling species Drosophila simulans and D. mauritiana. We mapped at least seven QTL affecting discrimination of D. mauritiana females against D. simulans males, three QTL affecting D. simulans male traits against which D. mauritiana females discriminate, and six QTL affecting D. mauritiana male traits against which D. simulans females discriminate. QTL affecting sexual isolation act additively, are largely different in males and females, and are not disproportionately concentrated on the X chromosome: The QTL of greatest effect are located on chromosome 3. Unlike the genetic components of postzygotic isolation, the loci for prezygotic isolation do not interact epistatically. The observation of a few QTL with moderate to large effects will facilitate positional cloning of genes underlying sexual isolation.
Male mating behavior is an important component of fitness in Drosophila and displays segregating variation in natural popluations. However, we know very little about the genes affecting naturally occurring variation in mating behavior, their effects, or their interactions. Here, we have mapped quantitative trait loci (QTL) affecting courtship occurrence, courtship latency, copulation occurrence, and copulation latency that segregate between a D. melanogaster strain selected for reduced male mating propensity (2b) and a standard wild-type strain (Oregon-R). Mating behavior was assessed in a population of 98 recombinant inbred lines derived from these two strains and QTL affecting mating behavior were mapped using composite interval mapping. We found four QTL affecting male mating behavior at cytological locations 1A;3E, 57C;57F, 72A;85F, and 96F;99A. We used deficiency complementation mapping to map the autosomal QTL with much higher resolution to five QTL at 56F5;56F8, 56F9;57A3, 70E1;71F4, 78C5;79A1, and 96F1;97B1. Quantitative complementation tests performed for 45 positional candidate genes within these intervals revealed 7 genes that failed to complement the QTL: eagle, 18 wheeler, Enhancer of split, Polycomb, spermatocyte arrest, l(2)05510, and l (2) result in altered rhythmicity in courtship song, and disand females, allowing for the individual components of ruptions in components of the sex-determination paththe behavior to be separated (Hall 1994; Greenspan way genes Sex-lethal (Sxl), transformer (tra), transformer-2 1995). First the male aligns himself with the female.(tra-2), or fruitless (fru; Cline 1993; Barbash and Cline Then he taps the female with his foreleg, performs a 1995; MacDougall et al. 1995;Finley et al. 1997; "courtship song" by vibrating one wing, extends his proSchü tt and Nö thiger 2000) result in altered sexual orientation. In Drosophila, male mating ability is a critical compo-1
A major unresolved challenge of evolutionary biology is to determine the nature of the allelic variants of ''speciation genes'': those alleles whose interaction produces inviable or infertile interspecific hybrids but does not reduce fitness in pure species. Here we map quantitative trait loci (QTL) affecting fertility of male hybrids between D. yakuba and its recently discovered sibling species, D. santomea. We mapped three to four X chromosome QTL and two autosomal QTL with large effects on the reduced fertility of D. yakuba and D. santomea backcross males. We observed epistasis between the X-linked QTL and also between the X and autosomal QTL. The X chromosome had a disproportionately large effect on hybrid sterility in both reciprocal backcross hybrids. However, the genetics of hybrid sterility differ between D. yakuba and D. santomea backcross males, both in terms of the magnitude of main effects and in the epistatic interactions. The QTL affecting hybrid fertility did not colocalize with QTL affecting sexual isolation in this species pair, but did colocalize with QTL affecting the marked difference in pigmentation between D. yakuba and D. santomea. These results provide the basis for future high-resolution mapping and ultimately, molecular cloning, of the interacting genes that contribute to hybrid sterility. U NDERSTANDING the genetic basis of speciation-the splitting of a group of interbreeding populations into two reproductively isolated groups-is a major challenge of evolutionary biology. Yet the framework in which we must seek to determine the genetic basis of postzygotic reproductive isolation-the inviability or sterility of interspecific offspring-has been clear from the beginning of the last century. First, hybrid dysfunction must be caused by deleterious epistatic interactions (''incompatibilities'') between genes that function perfectly well in pure-species backgrounds. Dobzhansky (1937) and Muller (1940) proposed a simple two-locus model that explains how such incompatibilities could arise if different alleles at the two loci become fixed in the two species. In this model, the ancestral species has genotype A 1 A 1 B 1 B 1 , and its two descendant species have genotypes A 1 A 1 B 2 B 2 and A 2 A 2 B 1 B 1 , respectively. There would be no selection against deleterious interactions between A 1 and A 2 or B 1 and B 2 in the pure species, but such interactions may exist between alleles A 1 and B 2 in the separate lineages, causing inviability or sterility of the A 1 A 2 B 1 B 2 hybrids.Second, Haldane (1922, p. 101) noted that: ''When in the F 1 offspring of two different animal races one sex is absent, rare, or sterile, that sex is the heterozygous [heterogametic] sex.'' One of the causes of Haldane's rule thus is likely to be incompatibilities involving the sex chromosomes with each other or with autosomes (other factors probably also contribute to Haldane's rule; see Coyne and Orr 2004).Thus, to understand the genetic architecture of postzygotic reproductive isolation, we must identify...
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