Department of Biological Sciences, University of Toledo, 2801 W. Bancroft St., MS601, BO3090, Toledo, OH, 43606, USA.
Johns Hopkins University, Department of Mechanical Engineering, Latrobe Hall 223, 3400 North Charles St., Baltimore, MD, 21218, USA.
Sci Rep. 2019 Mar 26;9(1):5163. doi: 10.1038/s41598-019-41558-7.
Focal adhesions (FA) are a complex network of proteins that allow the cell to form physical contacts with the extracellular matrix (ECM). FA assemble and disassemble in a dynamic process, orchestrated by a variety of cellular components. However, the underlying mechanisms that regulate adhesion turnover remain poorly understood. Here we show that RhoG, a Rho GTPase related to Rac, modulates FA dynamics. When RhoG expression is silenced, FA are more stable and live longer, resulting in an increase in the number and size of adhesions, which are also more mature and fibrillar-like. Silencing RhoG also increases the number and thickness of stress fibers, which are sensitive to blebbistatin, suggesting contractility is increased. The molecular mechanism by which RhoG regulates adhesion turnover is yet to be characterized, but our results demonstrate that RhoG plays a role in the regulation of microtubule-mediated FA disassembly.
焦点黏附（FA）是一种复杂的蛋白质网络，使细胞能够与细胞外基质（ECM）形成物理接触。FA 通过各种细胞成分的协调在一个动态过程中组装和解体。然而，调节黏附周转率的潜在机制仍知之甚少。在这里，我们表明 RhoG，一种与 Rac 相关的 Rho GTPase，调节 FA 的动态变化。当 RhoG 表达被沉默时，FA 更稳定且寿命更长，导致黏附物的数量和大小增加，并且更加成熟和纤维状。沉默 RhoG 还增加了应力纤维的数量和厚度，这些纤维对 blebbistatin 敏感，表明收缩性增加。RhoG 调节黏附物周转率的分子机制尚未确定，但我们的结果表明 RhoG 在微管介导的 FA 解体的调节中发挥作用。
