Sexual Dimorphism in the Drosophila Gonad

描述（由申请人提供）：生物学中的一个基本问题是在发育过程中如何产生不同的性表型，男性与女性。性腺的两性异形特别重要，因为性腺必须产生不同的雄性或雌性配子进行生殖，并且通常控制身体其他部位的性发育。男性和女性之间的选择是由性别决定“开关”启动的，这是一种控制性别认同的遗传或环境信号。性别决定开关可以在不同的动物物种之间有很大的差异。然而，有越来越多的证据表明，这些开关控制的途径，创造性的二型性可能是高度保守的，甚至在脊椎动物和无脊椎动物之间。 我们已经发现果蝇的性腺在最初的性腺形成时就已经是两性异形的了。一组体细胞被募集到发育中的睾丸中，而不是卵巢。有趣的是，这些细胞表达了果蝇Sox 9的同源物，Sox 9是一种对人类性别决定至关重要的基因，被认为在其他脊椎动物中起着类似的作用。雄性特异性细胞最初在两种性别中形成，但在雌性中通过程序性细胞死亡被消除。体细胞性腺中的两性异形也直接调节生殖细胞的雄性或雌性特异性发育。 我们的初步工作现在使我们能够解决几个关于性腺性二态性的基本问题：1）性别决定开关如何控制性二态性？2)男性特异性细胞进入性腺的募集如何影响睾丸的形成？3)果蝇Sox 9同源基因在雄性性发育中是否起保守作用？4)性特异性生殖细胞的发育如何受体细胞性腺的调控？这项工作将进一步加深我们对细胞和分子水平上两性异形是如何控制的理解。它还将为理解人类综合征提供基础，例如由Sox 9缺失引起的综合征，其中性二态性被破坏，导致性逆转和不育。

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.