Vinculin association with actin cytoskeleton is necessary for stiffness-dependent regulation of vinculin behavior.
Vinculin association with actin cytoskeleton is necessary for stiffness-dependent regulation of vinculin behavior.
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DOI：
10.1371/journal.pone.0175324
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Kioka N
中科院分区：
文献类型：
--
作者：
Omachi T;Ichikawa T;Kimura Y;Ueda K;Kioka N
细胞外基质（ECM）是细胞行为的主要调节因子。最近的研究表明，ECM的物理性质，包括其刚度，对细胞迁移和分化的重要性。使用肌动球蛋白产生的力，细胞拉动ECM并通过称为粘着斑（FA）的细胞-ECM粘附结构感知刚度。肌动蛋白结合FA蛋白，已成为FA介导的机械转导的主要参与者。虽然黏着斑蛋白是重要的传感ECM刚度，黏着斑蛋白结合肌动蛋白在ECM刚度介导的调节黏着斑蛋白的行为仍然是未知的。在这里，我们表明，肌动蛋白结合缺陷突变破坏CSB（细胞骨架稳定缓冲液）电阻和黏着斑蛋白的稳定本地化的ECM刚度依赖性调节。这些结果表明，长春纽蛋白-肌动蛋白相互作用参与FA介导的力学转导。
The extracellular matrix (ECM) is a major regulator of cell behavior. Recent studies have indicated the importance of the physical properties of the ECM, including its stiffness, for cell migration and differentiation. Using actomyosin-generated forces, cells pull the ECM and sense stiffness via cell-ECM adhesion structures called focal adhesions (FAs). Vinculin, an actin-binding FA protein, has emerged as a major player in FA-mediated mechanotransduction. Although vinculin is important for sensing ECM stiffness, the role of vinculin binding to actin in the ECM stiffness-mediated regulation of vinculin behavior remains unknown. Here, we show that an actin binding-deficient mutation disrupts the ECM stiffness-dependent regulation of CSB (cytoskeleton stabilization buffer) resistance and the stable localization of vinculin. These results suggest that the vinculin-actin interaction participates in FA-mediated mechanotransduction.