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类固醇信号传导控制一种无脊椎动物的性别特异性发育。

Steroid signaling controls sex-specific development in an invertebrate.

作者信息

Grmai Lydia, Jimenez Erin, Baxter Ellen, Doren Mark Van

机构信息

Department of Biology, Johns Hopkins University, Baltimore, Maryland, USA.

出版信息

bioRxiv. 2024 Jun 26:2023.12.22.573099. doi: 10.1101/2023.12.22.573099.

Abstract

In vertebrate sexual development, two important steroid hormones, testosterone and estrogen, regulate the sex-specific development of many tissues. In contrast, invertebrates utilize a single steroid hormone, ecdysone, to regulate developmental timing in both sexes. However, here we show that in , sex-specific ecdysone (E) signaling controls important aspects of gonad sexual dimorphism. Rather than being regulated at the level of hormone production, hormone activity is regulated cell-autonomously through sex-specific hormone reception. Ecdysone receptor (EcR) expression is restricted to the developing ovary and is repressed in the testis at a time when ecdysone initiates ovary morphogenesis. Interestingly, EcR expression is regulated downstream of the sex determination factor Doublesex (Dsx), the founding member of the Dsx/Mab3 Related Transcription Factor (DMRT) family that regulates gonad development in all animals. E signaling is required for normal ovary development, and ectopic activation of E signaling in the testis antagonized stem cell niche identity and feminized somatic support cells, which were transformed into follicle-like cells. This work demonstrates that invertebrates can also use steroid hormone signaling to control sex-specific development. Further, it may help explain recent work showing that vertebrate sexual development is surprisingly cell-autonomous. For example, chickens utilize testosterone and estrogen to control sex-specific development, but when they have a mixture of cells with male and female genotypes, the male cells develop as male and the female cells develop as female despite exposure to the same circulating hormones. Sex-specific regulation of steroid hormone signaling may well underly such cell-autonomous sexual fate choices in vertebrates as it does in .

摘要

在脊椎动物性发育过程中,两种重要的类固醇激素——睾酮和雌激素,调节着许多组织的性别特异性发育。相比之下,无脊椎动物利用单一的类固醇激素蜕皮激素来调节两性的发育时间。然而,我们在此表明,在[具体物种未提及]中,性别特异性的蜕皮激素(E)信号传导控制着性腺性二态性的重要方面。激素活性并非在激素产生水平上受到调节,而是通过性别特异性的激素受体在细胞自主水平上受到调节。蜕皮激素受体(EcR)的表达仅限于发育中的卵巢,在蜕皮激素启动卵巢形态发生时,其在睾丸中受到抑制。有趣的是,EcR的表达受性别决定因子双性(Dsx)的下游调控,Dsx是Dsx/Mab3相关转录因子(DMRT)家族的创始成员,该家族在所有动物中调节性腺发育。E信号传导是正常卵巢发育所必需的,睾丸中E信号的异位激活拮抗了干细胞微环境身份,并使体细胞支持细胞雌性化,这些细胞转化为卵泡样细胞。这项工作表明,无脊椎动物也可以利用类固醇激素信号传导来控制性别特异性发育。此外,它可能有助于解释最近的研究结果,即脊椎动物性发育惊人地具有细胞自主性。例如,鸡利用睾酮和雌激素来控制性特异性发育,但当它们具有雄性和雌性基因型混合的细胞时,尽管暴露于相同的循环激素中,雄性细胞仍发育为雄性,雌性细胞仍发育为雌性。类固醇激素信号传导的性别特异性调节很可能是脊椎动物中这种细胞自主性性别命运选择的基础,就像在[具体物种未提及]中一样。

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