Sexual Dimorphism in the Drosophila Gonad

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DESCRIPTION (provided by applicant): A fundamental problem in biology is how different sexual phenotypes, male vs. female, are created during development. Sexual dimorphism in the gonad is particularly important, since the gonad must generate distinct male or female gametes for reproduction, and often controls the sexual development of other parts of the body. The choice between male and female is initiated by a sex determination "switch", a genetic or environmental signal that controls sexual identity. Sex determination switches can vary widely between different animal species. However, there is increasing evidence that the pathways these switches control to create sexual dimorphism may be more highly conserved, even between vertebrates and invertebrates. We have found that the Drosophila gonad is already sexually dimorphic at the time of initial gonad formation. A group of somatic cells is recruited into the developing testis, but not the ovary. Interestingly, these cells express a Drosophila homolog of Sox9, a gene that is critical for sex determination in humans and is thought to play a similar role in other vertebrates. The male-specific cells initially form in both sexes, but are eliminated in the female by programmed cell death. Sexual dimorphism in the somatic gonad also directly regulates male- or female-specific development of the germ cells. Our initial work now enables us to address several essential questions about gonad sexual dimorphism: 1) How does a sex determination switch control sexual dimorphism? 2) How does the recruitment of male-specific cells into the gonad influence testis formation? 3) Does the Drosophila Sox9 homolog play a conserved role in male sexual development? 4) How is sex-specific germ cell development regulated by the somatic gonad? This work will further our understanding of how sexual dimorphism is controlled at the cellular and molecular levels. It will also provide a basis for understanding human syndromes, such as the one caused by loss of Sox9, where sexual dimorphism is disrupted, resulting in sex reversal and infertility.