| Speciation---an important cause of biodiversity---occurs by the evolution of reproductive isolation between populations. Reproductive isolation can be achieved by many means, including intrinsic postzygotic isolation, the inviability or sterility of species hybrids. Although much is known about the general patterns characterizing the genetics of postzygotic isolation, several questions about its molecular causes remain unanswered. Here, I present three studies that investigate some of these outstanding questions by taking advantage of the genetic tools available in Drosophila.; In the first study, I investigate a controversial pattern that may or may not characterize the genetics of postzygotic isolation: the large X-effect. I perform a genome-wide introgression analysis between two closely related species to test the effects of X-linked versus autosomal introgressions on postzygotic isolation. I also molecularly estimate and compare introgression sizes between the X and the autosomes. My results show that the X has a disproportionately large effect on hybrid male sterility compared to the effects of similarly sized autosomes; this effect is not confounded by any bias in introgression size. These results demonstrate conclusively the existence of the large X-effect, and show that its proximate cause is a higher density of hybrid male-steriles on the X chromosome compared to the autosomes.; In the second study, I fine-map and identify a gene that causes hybrid male sterility in Drosophila. In the course of this work, I uncover evidence for a novel mechanism of reproductive isolation. Postzygotic isolation usually evolves as a result of incompatible epistatic interactions between functionally diverged loci. Surprisingly, however, JYAlpha ---a single-copy, fertility-essential gene---causes complete hybrid sterility because of a change in chromosomal location between species, not because of a change in function.; In the third study, I investigate a different postzygotic hybrid fitness problem: sex-ratio distortion. I map some of the genes necessary for the expression of sex-ratio distortion in D. simulans-D. sechellia hybrids, and find that at least three of the required regions reside on chromosome 3 whereas none resides on chromosome 2. I also find no obvious cytological abnormalities in sperm from hybrid males that might suggest the proximate cause of sex-ratio distortion. |
