Rho family GTPase functions in Drosophila epithelial wound repair.
Rho family GTPase functions in Drosophila epithelial wound repair.
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DOI：
10.4161/21541248.2014.982415
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Parkhurst SM
中科院分区：
文献类型：
--
作者：
Verboon JM;Parkhurst SM
果蝇胚胎中的上皮修复是通过两种动态细胞骨架机制实现的：收缩性肌动球蛋白线和基于肌动蛋白的细胞突起。 Rho 家族小 GTP 酶（Rho、Rac 和 Cdc42）是控制这两种伤口修复机制的细胞骨架调节因子。 Cdc42 对于细胞突起是必需的，如果不存在，伤口修复缓慢且永远无法完全闭合。 Rac 蛋白在伤口前缘细胞的特定区域积聚，并且 Rac 缺陷胚胎表现出较慢的修复动力学。 Rho1 及其效应器 Rok 的突变体会破坏前沿肌动蛋白线，从而损害伤口闭合的能力。我们的研究强调了这些蛋白质在伤口修复中的重要性，并确定了该过程中 Rho1 信号传导的下游效应子。
Epithelial repair in the Drosophila embryo is achieved through 2 dynamic cytoskeletal machineries: a contractile actomyosin cable and actin-based cellular protrusions. Rho family small GTPases (Rho, Rac, and Cdc42) are cytoskeletal regulators that control both of these wound repair mechanisms. Cdc42 is necessary for cellular protrusions and, when absent, wounds are slow to repair and never completely close. Rac proteins accumulate at specific regions in the wound leading edge cells and Rac-deficient embryos exhibit slower repair kinetics. Mutants for both Rho1 and its effector Rok impair the ability of wounds to close by disrupting the leading-edge actin cable. Our studies highlight the importance of these proteins in wound repair and identify a downstream effector of Rho1 signaling in this process.