Distinct roles of Bendless in regulating FSC niche competition and daughter cell differentiation.
Distinct roles of Bendless in regulating FSC niche competition and daughter cell differentiation.
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DOI：
10.1242/dev.199630
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发表时间：
2021-11
期刊：
影响因子：
4.6
通讯作者：
Sumitra Tatapudy;Jobelle Peralta;T. Nystul
中科院分区：
文献类型：
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作者：
Sumitra Tatapudy;Jobelle Peralta;T. Nystul
成体干细胞研究的一个主要目标是了解如何在适当的时间和地点指定细胞命运以促进组织稳态。在这里，我们发现E2泛素连接酶Bendless （Ben）在果蝇卵巢上皮卵泡干细胞（FSC）谱系中具有多种作用。首先，Ben是JNK信号通路的一部分，我们发现它和其他JNK通路基因一样，对于FSC子细胞的分化是必不可少的。我们的数据表明，JNK信号通过抑制EGFR效应物ERK的激活来促进分化。此外，我们发现ben的缺失，而不是JNK激酶的缺失，导致刺猬信号的上调，增殖增加和利基竞争增加。最后，我们证明了由ben缺失引起的超竞争表型可以通过降低增殖速率或敲低hedgehog通路效应物Smoothened （Smo）来抑制。综上所述，我们的发现揭示了一个新的调控层，其中单个基因影响早期FSC谱系中分化的多个阶段的细胞信号传导。
A major goal in the study of adult stem cells is to understand how cell fates are specified at the proper time and place to facilitate tissue homeostasis. Here, we found that an E2 ubiquitin ligase, Bendless (Ben), has multiple roles in the Drosophila ovarian epithelial follicle stem cell (FSC) lineage. First, Ben is part of the JNK signaling pathway, and we found that it, as well as other JNK pathway genes, are essential for differentiation of FSC daughter cells. Our data suggest that JNK signaling promotes differentiation by suppressing the activation of the EGFR effector, ERK. Also, we found that loss of ben, but not the JNK kinase hemipterous, resulted in an upregulation of hedgehog signaling, increased proliferation and increased niche competition. Lastly, we demonstrate that the hypercompetition phenotype caused by loss of ben is suppressed by decreasing the rate of proliferation or knockdown of the hedgehog pathway effector, Smoothened (Smo). Taken together, our findings reveal a new layer of regulation in which a single gene influences cell signaling at multiple stages of differentiation in the early FSC lineage.