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Abstract：
As collective cell migration is intimately involved in different aspects of metazoan development, molecular mechanisms underlying this process are being explored in a variety of developmental contexts. Border cell (BC) migration during Drosophila oogenesis has emerged as an excellent genetic model for studying collective cell migration. BCs are of epithelial origin but acquire partial mesenchymal characteristics before migrating as a group towards the oocyte. Here, we report that insulin signaling modulates collective BC movement during Drosophila oogenesis. Supporting the involvement of Insulin pathway, we demonstrate that compromising Insulin-like Receptor (InR) levels in BCs, inhibits their migration. Furthermore, we show that canonical Insulin signaling pathway components participate in this process. Interestingly, visualization of InR-depleted BC clusters, using time-lapse imaging, revealed a delay in detachment of BC clusters from the surrounding anterior follicle cells and altered protrusion dynamics. Lastly, based on genetic interactions between InR, the polarity determinant, par-1 and a regulatory subunit of Drosophila Myosin (spaghetti squash), we propose that Insulin signaling likely influences par-1 activity to engineer border cell detachment and subsequent movement via Drosophila Myosin.
摘要：
由于集体细胞迁移与后生动物发育的不同方面密切相关，这一过程背后的分子机制正在各种发展环境中进行探索。果蝇卵子发生过程中的边界细胞（BC）迁移已成为研究集体细胞迁移的出色遗传模型。BCs是上皮起源的，但在作为一组向卵母细胞迁移之前获得部分间充质特征。这里,我们报道了胰岛素信号调节果蝇卵子发生过程中的集体BC运动。支持胰岛素途径的参与，我们证明了BCs中胰岛素样受体（InR）水平的下降，抑制他们的迁移。此外，我们证明了典型的胰岛素信号通路成分参与了这一过程。有趣的是,InR耗尽的BC簇的可视化，使用延时成像，显示BC簇与周围前卵泡细胞的脱离延迟，并改变了突起动力学。最后,基于InR之间的遗传相互作用，极性决定因素，par-1和果蝇肌球蛋白（意大利南瓜）的调节亚基，我们认为胰岛素信号传导可能通过果蝇肌球蛋白影响par-1活性,从而设计边界细胞脱离和随后的运动。
