Massachusetts Institute of Technology, David H. Koch Institute for Integrative Cancer Research, 77 Massachusetts Ave, 76-361F, Cambridge, MA 02139-4307, United States.
The University of Chicago, Department of Molecular Genetics and Cell Biology, 90 E. 58th Street, CSLC 212, Chicago, IL 60637, United States.
Curr Opin Cell Biol. 2019 Feb;56:130-140. doi: 10.1016/j.ceb.2018.12.008. Epub 2019 Jan 11.
Fundamental cellular processes such as division, polarization, and motility require the tightly regulated spatial and temporal assembly and disassembly of the underlying actin cytoskeleton. The actin cytoskeleton has been long viewed as a central player facilitating diverse mechanotransduction pathways due to the notion that it is capable of receiving, processing, transmitting, and generating mechanical stresses. Recent work has begun to uncover the roles of mechanical stresses in modulating the activity of key regulatory actin-binding proteins and their interactions with actin filaments, thereby controlling the assembly (formin and Arp2/3 complex) and disassembly (ADF/Cofilin) of actin filament networks. In this review, we will focus on discussing the current molecular understanding of how members of the formin protein family sense and respond to forces and the potential implications for formin-mediated mechanotransduction in cells.
基本的细胞过程，如分裂、极化和运动，需要严格调节基础肌动蛋白细胞骨架的空间和时间组装和拆卸。由于肌动蛋白细胞骨架能够接收、处理、传递和产生机械应力，因此它一直被视为促进多种机械转导途径的核心参与者。最近的工作开始揭示机械应力在调节关键调节肌动蛋白结合蛋白的活性及其与肌动蛋白丝相互作用中的作用，从而控制肌动蛋白丝网络的组装（formin 和 Arp2/3 复合物）和拆卸（ADF/Cofilin）。在这篇综述中，我们将重点讨论当前对formin 蛋白家族成员如何感知和响应力的分子理解，以及这对细胞中介导的机械转导的潜在影响。
