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The small GTPase Rif is an alternative trigger for the formation of actin stress fibers in epithelial cells

机译:小的GTPase Rif是上皮细胞中肌动蛋白应激纤维形成的另一种触发机制

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摘要

Actin stress fibers are fundamental components of the actin cytoskeleton that produce contractile force in non-muscle cells. The formation of stress fibers is controlled by the small GTPase RhoA and two highly related proteins, RhoB and RhoC. Together, this subgroup of actin-regulatory proteins represents the canonical pathway of stress-fiber formation. Here, we show that the Rif GTPase is an alternative trigger of stress-fiber formation in epithelial cells. Rif is distantly related to RhoA; however, we show that the two proteins share a common downstream partner in stress-fiber formation – the Diaphanous-related formin mDia1. Rif-induced stress fibers also depend on the activity of the ROCK protein kinase. Unlike RhoA, Rif does not raise ROCK activity in cells, instead Rif appears to regulate the localization of myosin light chain phosphorylation. This study establishes Rif as a general regulator of Diaphanous-related formins and shows how non-classical Rho family members can access classical Rho pathways to create new signaling interfaces in cytoskeletal regulation.
机译:肌动蛋白应激纤维是肌动蛋白细胞骨架的基本组成部分,可在非肌肉细胞中产生收缩力。应力纤维的形成由小的GTPase RhoA和两个高度相关的蛋白质RhoB和RhoC控制。肌动蛋白调节蛋白这一亚组共同代表了应力纤维形成的典型途径。在这里,我们显示Rif GTPase是上皮细胞中应力纤维形成的另一种触发方式。 Rif与RhoA密切相关;但是,我们证明了这两种蛋白质在应力纤维形成过程中共享一个共同的下游伙伴-透照相关的甲酰胺mDia1。 Rif诱导的应激纤维还取决于ROCK蛋白激酶的活性。与RhoA不同,Rif不会提高细胞中的ROCK活性,而Rif似乎可以调节肌球蛋白轻链磷酸化的位置。这项研究将Rif确立为与透辉有关的formins的一般调节物,并展示了非经典Rho家族成员如何能够访问经典Rho途径以在细胞骨架调节中创建新的信号传导界面。

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