Wnt Signaling in Sexual Dimorphism
Wnt Signaling in Sexual Dimorphism
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DOI：
10.1534/genetics.115.177857
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发表时间：
2016-02-01
期刊：
影响因子：
3.3
通讯作者：
Schedl, Paul
中科院分区：
文献类型：
--
作者：
Deshpande, Girish;Nouri, Ali;Schedl, Paul
黑腹果蝇的胚胎性腺在形成后不久就开始表现出性别二态特征。在这里，我们证明了WNT家族配体WNT-2参与了这些性别差异的诱导。我们发现WNT-2有助于男性特定的体细胞性腺前体细胞(SGPS)群体的存活，SGPS是位于男性性腺后部的男性特定的SGPS。我们还发现Wnt-2配体与JAK-STAT配体UPD协同作用，后者是由SGPS在性腺前部产生的，激活男性生殖细胞中的STAT通路。我们认为，使用两个空间上分离的信号系统来启动生殖细胞中的JAK-STAT干细胞维持途径，为增加成人睾丸中生殖系干细胞的潜在祖细胞提供了一种机制。最后，我们提出的证据表明，像JAK-STAT通路一样，WNT-2刺激男性胚胎中的生殖细胞重新进入细胞周期。
The embryonic gonad of Drosophila melanogaster begins to display sexually dimorphic traits soon after its formation. Here we demonstrate the involvement of a wnt family ligand, wnt-2, in the induction of these sex-specific differences. We show that wnt-2 contributes to the survival of a male-specific population of somatic gonadal precursor cells (SGPs), the male-specific SGPs that are located at the posterior of the male gonad. We also show that the Wnt-2 ligand synergizes with the JAK-STAT ligand Upd, which is produced by SGPs at the anterior of the gonad to activate the STAT pathway in male germ cells. We suggest that the use of two spatially separated signaling systems to initiate the JAK-STAT stem cell maintenance pathway in germ cells provides a mechanism for increasing the pool of potential progenitors of the germline stem cells in the adult testes. Finally, we present evidence indicating that, like the JAK-STAT pathway, wnt-2 stimulates germ cells in male embryos to re-enter the cell cycle.