Mating-Induced Increase in Germline Stem Cells via the Neuroendocrine System in Female Drosophila.
Mating-Induced Increase in Germline Stem Cells via the Neuroendocrine System in Female Drosophila.
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DOI：
10.1371/journal.pgen.1006123
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发表时间：
2016-06
期刊：
影响因子：
4.5
通讯作者：
Niwa R
中科院分区：
文献类型：
--
作者：
Ameku T;Niwa R
交配和配子发生是动物繁殖的两个基本组成部分。配子发生必须通过对配子的需要来调节，但很少有人知道交配是如何利用配子的过程，可以调节配子发生的过程。在这里，我们报告说，交配刺激雌性生殖干细胞（GSC）在果蝇增殖。交配诱导的GSC数量的增加不仅仅是由于储存的卵子的排放的间接作用，而是由雄性衍生的性肽（SP）及其受体SPR刺激的，这是诱导雌性交配后行为转换的典型神经元通路的组成部分。我们发现，蜕皮激素，主要的昆虫类固醇激素，调节交配诱导的GSC增殖独立的胰岛素信号。交配后卵巢蜕皮激素水平增加，并通过卵巢小生境中表达的蜕皮激素受体直接传递其信号，以增加GSC的数量。卵巢蜕皮激素生物合成的受损会破坏交配诱导的GSC增加以及卵子产量。重要的是，喂食蜕皮激素可以挽救神经元SP信号传导受损引起的GSC数量减少。我们的研究说明了女性GSC的活动是如何协调调节的神经内分泌系统，以维持生殖成功的交配。在许多动物中，配子发生由生殖系干细胞（GSC）支持。由于GSC是成功繁殖的基本细胞群，因此这种特殊的GSC如何精确增殖是生物学中一个长期存在的问题。在果蝇Drosophila melanogaster中，已知配子发生受环境条件和外部刺激影响。然而，目前尚不清楚GSC增殖是如何在分子和细胞水平上响应于这些外部信号而调节的。在这里，我们报告说，交配刺激女性卵巢干细胞的活动。交配通过雄性衍生的性肽（SP）刺激的神经元信号传导诱导GSC增殖。SP依赖性GSC增殖受蜕皮激素（昆虫主要类固醇激素）控制，独立于胰岛素信号传导。本研究的意义在于阐明神经内分泌调节机制在交配后GSC增殖中的作用，这可能有助于持续和适应性地产生卵子。此外，我们的研究结果将打开一扇大门，对动物行为（交配）和干细胞调控之间不可或缺的机械联系有新的理解。
Mating and gametogenesis are two essential components of animal reproduction. Gametogenesis must be modulated by the need for gametes, yet little is known of how mating, a process that utilizes gametes, may modulate the process of gametogenesis. Here, we report that mating stimulates female germline stem cell (GSC) proliferation in Drosophila melanogaster. Mating-induced increase in GSC number is not simply owing to the indirect effect of emission of stored eggs, but rather is stimulated by a male-derived Sex Peptide (SP) and its receptor SPR, the components of a canonical neuronal pathway that induces a post-mating behavioral switch in females. We show that ecdysteroid, the major insect steroid hormone, regulates mating-induced GSC proliferation independently of insulin signaling. Ovarian ecdysteroid level increases after mating and transmits its signal directly through the ecdysone receptor expressed in the ovarian niche to increase the number of GSCs. Impairment of ovarian ecdysteroid biosynthesis disrupts mating-induced increase in GSCs as well as egg production. Importantly, feeding of ecdysteroid rescues the decrease in GSC number caused by impairment of neuronal SP signaling. Our study illustrates how female GSC activity is coordinately regulated by the neuroendocrine system to sustain reproductive success in response to mating. In many animals, gametogenesis is supported by germline stem cells (GSCs). Since GSCs are the fundamental cell population for successful reproduction, how such special GSCs are precisely proliferated is a long-standing question in biology. In the fruit fly Drosophila melanogaster, it is known that gametogenesis is affected by environmental conditions and external stimuli. However, it remains unclear how GSC proliferation is regulated in response to such external signals at the molecular and cellular levels. Here, we report that mating stimulates stem cell activity in female ovary. Mating induces GSC proliferation via neuronal signaling stimulated by a male-derived Sex Peptide (SP). SP-dependent GSC proliferation is controlled by the ecdysteroid, the major insect steroid hormone, independently of insulin signaling. A significance of our study is to illustrate a role of the neuroendocrine regulatory mechanism in the GSC proliferation after mating, which might contribute to continuously and adaptively producing eggs. Furthermore, our findings will open the door to a new understanding of an indispensable mechanistic link between animal behavior (mating) and the regulation of stem cells.