Throughout the animal kingdom, sex-specific development is used to create different forms in males and females. Sexual dimorphism is important for successful reproduction both on social and biological levels, but is especially vital in the gonad, which must be sexually dimorphic so it can support germline differentiation into sperm and eggs. In Drosophila, adult testes and ovaries are highly specialized organs that can serve as good models for studying sex-specific gonadogenesis, however, it is not well understood how sexual dimorphism is initially established in the embryo. In this thesis I present an analysis of how differences between the male and female somatic gonad are brought about during early development. I have observed that the Drosophila gonad is already sexually dimorphic at the time of its initial formation, and have characterized two sex-specific cell types termed the male-specific somatic gonadal precursors (msSGPs) and the pigment cell precursors. msSGPs and pigment cells give rise to specific adult testis cell types and express Sox100B, a homolog of Sox9, a factor required for mammalian sex determination. These two cell types employ different cellular mechanisms, such as apoptosis and cell-cell signaling, to ensure sexual dimorphism in the gonad. Sex-specific gonad development relies on positional information provided by the homeotic genes and proper sexual identity downstream of the sex determination gene doublesex. The sexually dimorphic behavior of msSGPs and pigment cells appears to be controlled non-autonomously, which is distinct from cell-autonomous sex determination that has been reported for most other Drosophila somatic tissues. Finally, I have analyzed the function of Sox100B in gonad development, and have found a role in adult iii testis formation, suggesting that there is a conserved molecular mechanism for regulating sexual dimorphism between flies and mammals. These results demonstrate many common features between Drosophila and mammalian gonadogenesis. Thus, despite vast differences in initial sex determination between species, these data strongly support a hypothesis that the downstream regulation of sexual dimorphism in the gonad is an evolutionarily conserved process at the cellular and molecular levels.
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