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Non-autonomous role of Cdc42 in cell-cell communication during collective migration

机译:CDC42在集体迁移期间CDC42在细胞 - 细胞通信中的非自主作用

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摘要

Collective cell migration is involved in numerous processes both physiological, such as embryonic development, and pathological such as metastasis. Compared to single cell migration, collective motion requires cell behaviour coordination through an as-yet poorly understood but critical cell-cell communication mechanism. Using Drosophila border cell migration, we show here that the small Rho GTPase Cdc42 regulates cell-cell communication. Indeed, we demonstrate that Cdc42 controls protrusion formation in a cell non-autonomous manner. Moreover, we found that the endocytic small GTPase Rab11, controls Cdc42 localisation to the periphery of migrating border cell clusters. Accordingly, over-expression of Cdc42 in border cells rescues the loss of Rabl I function. In addition, we showed that Cdc42 acts upstream of Moesin, a cytoskeletal regulator known to function downstream of rabl 1. Thus, our study positions Cdc42 as a new key player in cell-cell communication, acting downstream of Rab11.
机译:集体细胞迁移涉及生理,例如胚胎发育的许多工艺和病态,例如转移。 与单细胞迁移相比,集体运动需要通过尚未理解但关键的细胞单元通信机制来进行细胞行为协调。 使用果蝇边界细胞迁移,我们在此显示小Rho GTPase CDC42调节细胞间通信。 实际上,我们证明了CDC42以细胞非自主方式控制突起形成。 此外,我们发现内吞的小GTP酶Rab11,控制CDC42定位到迁移边界细胞簇的周边。 因此,边界细胞中CDC42的过表达抵押了RABL I功能的损失。 此外,我们表明CDC42作用于Moesin的上游,一种已知的细胞骨架调节剂,其在Rabl1下游功能。因此,我们的研究将CDC42作为细胞 - 细胞通信中的新关键参与者,作用下游。

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