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Sexual Dimorphism in the Drosophila Gonad

Sexual Dimorphism in the Drosophila Gonad
果蝇性腺的性别二态性
批准号:
7032273
负责人:
Mark B Van Doren
金额:
$27.74万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2004
资助国家:
美国
项目状态:
已结题
起止时间:
2004-04-01 至 2009-03-31

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中文摘要
翻译
描述(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别表型,男性和女性。性腺中的性二型性尤其重要,因为性腺必须产生不同的雄配子或雌配子才能繁殖,并经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,性别决定“开关”是一种控制性别认同的遗传或环境信号。性别决定的开关在不同的动物物种之间可能会有很大的差异。然而,越来越多的证据表明,即使在脊椎动物和无脊椎动物之间,这些开关控制的创造性别二型性的途径可能也更加保守。 我们发现,果蝇的性腺在最初的性腺形成时就已经是二型性的。一组体细胞被招募到发育中的睾丸,但不是卵巢。有趣的是,这些细胞表达果蝇Sox9的同源物,Sox9是人类性别决定的关键基因,被认为在其他脊椎动物中扮演着类似的角色。雄性特有的细胞最初在两性中形成,但在雌性中被程序性细胞死亡消除。体细胞性腺中的性二型性也直接调节生殖细胞的男性或女性特有的发育。 我们的初步工作现在使我们能够解决性腺性二型性的几个基本问题:1)性别决定开关如何控制性二型性?2)性腺中男性特有细胞的招募如何影响睾丸的形成?3)果蝇Sox9同源基因在男性性发育中扮演着保守的角色吗?4)性特异性生殖细胞发育是如何受体细胞性腺调控的?这项工作将进一步加深我们对如何在细胞和分子水平上控制性二型性的理解。它还将为理解人类综合征提供基础,例如由Sox9基因缺失引起的综合征,即性二型性被破坏,导致性逆转和不孕。
英文摘要
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.
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Cellular and Molecular Biology
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