gone early, a novel germline factor, ensures the proper size of the stem cell precursor pool in the Drosophila ovary.
gone early, a novel germline factor, ensures the proper size of the stem cell precursor pool in the Drosophila ovary.
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DOI：
10.1371/journal.pone.0113423
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Asaoka M
中科院分区：
文献类型：
--
作者：
Matsuoka S;Gupta S;Suzuki E;Hiromi Y;Asaoka M
为了维持配子的终身生产，许多动物已经进化出基于干细胞的配子发生程序。在果蝇卵巢中，生殖系干细胞（GSC）来自原始生殖细胞（PGCs）池，即使在配子发生开始后仍保持未分化。PGC分化或保持未分化的决定由体细胞基质细胞调节：具体地，基质细胞中激活的表皮生长因子受体（EGFR）信号传导通过形成抑制PGC分化的十肢麻痹（Dpp）梯度来决定保持未分化的生殖细胞的分数。然而，关于生殖细胞在这一过程中的作用知之甚少。在这里，我们表明，一种新的生殖系因素，早去（Goe），限制部分的原始生殖细胞启动配子发生。goe编码Neprilysin家族金属内肽酶的非肽酶同系物。在配子发生开始时，Goe定位于卵巢中的生殖细胞膜上，这表明它在细胞表面的细胞-细胞通讯中以不依赖肽酶的方式起作用。生殖细胞中Goe的过表达减少了进入配子发生途径的PGCs的数量，从而增加了未分化PGCs的比例。然而，Goe的消耗增加了启动分化的PGCs的数量。goe突变体中的过度PGC分化通过将argos剂量减半而增强，argos是EGFR信号传导的体细胞表达抑制剂。这种PGC分化的增加导致未分化PGC数量的大量减少，并最终导致GSC形成不足。因此，与EGFR信号传导的体细胞调节因子合作，生殖系因子goe在确保GSC前体库的适当大小方面起关键作用。因为goe可以抑制EGFR信号传导活性，并且在各种组织中的EGF产生细胞中表达，所以goe可能通过减弱EGFR信号传导起作用，从而影响基质环境。
In order to sustain lifelong production of gametes, many animals have evolved a stem cell–based gametogenic program. In the Drosophila ovary, germline stem cells (GSCs) arise from a pool of primordial germ cells (PGCs) that remain undifferentiated even after gametogenesis has initiated. The decision of PGCs to differentiate or remain undifferentiated is regulated by somatic stromal cells: specifically, epidermal growth factor receptor (EGFR) signaling activated in the stromal cells determines the fraction of germ cells that remain undifferentiated by shaping a Decapentaplegic (Dpp) gradient that represses PGC differentiation. However, little is known about the contribution of germ cells to this process. Here we show that a novel germline factor, Gone early (Goe), limits the fraction of PGCs that initiate gametogenesis. goe encodes a non-peptidase homologue of the Neprilysin family metalloendopeptidases. At the onset of gametogenesis, Goe was localized on the germ cell membrane in the ovary, suggesting that it functions in a peptidase-independent manner in cell–cell communication at the cell surface. Overexpression of Goe in the germline decreased the number of PGCs that enter the gametogenic pathway, thereby increasing the proportion of undifferentiated PGCs. Inversely, depletion of Goe increased the number of PGCs initiating differentiation. Excess PGC differentiation in the goe mutant was augmented by halving the dose of argos, a somatically expressed inhibitor of EGFR signaling. This increase in PGC differentiation resulted in a massive decrease in the number of undifferentiated PGCs, and ultimately led to insufficient formation of GSCs. Thus, acting cooperatively with a somatic regulator of EGFR signaling, the germline factor goe plays a critical role in securing the proper size of the GSC precursor pool. Because goe can suppress EGFR signaling activity and is expressed in EGF-producing cells in various tissues, goe may function by attenuating EGFR signaling, and thereby affecting the stromal environment.
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