State Key Laboratory of Microbial Metabolism, School of Life Sciences & Biotechnology, The Joint International Research Laboratory of Metabolic & Developmental Sciences, Shanghai Jiao Tong University, Shanghai, 200240, China.
School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China.
Sci Rep. 2019 Jul 12;9(1):10124. doi: 10.1038/s41598-019-45317-6.
Stem cell self-renewal and the daughter cell differentiation are tightly regulated by the respective niches, which produce extrinsic cues to support the proper development. In Drosophila ovary, Dpp is secreted from germline stem cell (GSC) niche and activates the BMP signaling in GSCs for their self-renewal. Escort cells (ECs) in differentiation niche restrict Dpp outside the GSC niche and extend protrusions to help with proper differentiation of the GSC daughter cells. Here we provide evidence that loss of large Maf transcriptional factor Traffic jam (Tj) blocks GSC progeny differentiation. Spatio-temporal specific knockdown experiments indicate that Tj is required in pre-adult EC lineage for germline differentiation control. Further molecular and genetic analyses suggest that the defective germline differentiation caused by tj-depletion is partly attributed to the elevated dpp in the differentiation niche. Moreover, our study reveals that tj-depletion induces ectopic En expression outside the GSC niche, which contributes to the upregulated dpp expression in ECs as well as GSC progeny differentiation defect. Alternatively, loss of EC protrusions and decreased EC number elicited by tj-depletion may also partially contribute to the germline differentiation defect. Collectively, our findings suggest that Tj in ECs regulates germline differentiation by controlling the differentiation niche characteristics.
干细胞的自我更新和子细胞的分化受到各自的龛位的严格调控，龛位产生外在的信号来支持适当的发育。在果蝇卵巢中，Dpp 从生殖干细胞（GSC）龛位分泌，并在 GSCs 中激活 BMP 信号通路以维持其自我更新。分化龛位中的 escort 细胞（ECs）将 Dpp 限制在 GSC 龛位之外，并延伸突起，以帮助 GSC 子细胞的正常分化。在这里，我们提供的证据表明，大 Maf 转录因子 Traffic jam（Tj）的缺失会阻止 GSC 后代的分化。时空特异性敲低实验表明，Tj 在成虫前 EC 谱系中对于生殖细胞分化的控制是必需的。进一步的分子和遗传分析表明，tj 耗竭引起的生殖细胞分化缺陷部分归因于分化龛位中 dpp 的升高。此外，我们的研究表明，tj 耗竭诱导 GSC 龛位外的 En 表达异位，这导致 ECs 以及 GSC 后代分化缺陷中 dpp 表达的上调。另外，tj 耗竭引起的 EC 突起缺失和 EC 数量减少也可能部分导致生殖细胞分化缺陷。总之，我们的研究结果表明，EC 中的 Tj 通过控制分化龛位的特征来调节生殖细胞的分化。
