Liu B P, Chrzanowska-Wodnicka M, Burridge K
Department of Cell Biology and Anatomy, University of North Carolina, Chapel Hill 27599, USA.
Cell Adhes Commun. 1998 Jun;5(4):249-55. doi: 10.3109/15419069809040295.
Microtubule depolymerization has multiple consequences that include actin stress fiber and focal adhesion assembly, increased tyrosine phosphorylation and DNA synthesis. Similar effects induced by serum, or agents such as lysophosphatidic acid, have previously been shown to be mediated by the GTP-binding protein Rho. We have investigated whether the effects of microtubule depolymerization are similarly mediated by Rho and show that they are blocked by the specific Rho inhibitor, C3 transferase. Because microtubule depolymerization induces these effects in quiescent cells, in which Rho is largely inactive, we conclude that microtubule depolymerization leads to activation of Rho. The activation of Rho in response to microtubule depolymerization and the consequent stimulation of contractility suggest a mechanism by which microtubules may regulate microfilament function in various motile phenomena. These range from growth cone extension to the development of the contractile ring during cytokinesis, in which there are interactions between the microtubule and microfilament systems.
微管解聚有多种后果，包括肌动蛋白应力纤维和粘着斑组装、酪氨酸磷酸化增加以及DNA合成。血清或溶血磷脂酸等试剂诱导的类似效应先前已表明是由GTP结合蛋白Rho介导的。我们研究了微管解聚的效应是否同样由Rho介导，并表明它们被特异性Rho抑制剂C3转移酶阻断。由于微管解聚在静止细胞中诱导这些效应，而在静止细胞中Rho基本无活性，我们得出结论，微管解聚导致Rho激活。Rho对微管解聚的激活以及随之而来的收缩性刺激提示了一种机制，通过该机制微管可能在各种运动现象中调节微丝功能。这些现象从生长锥延伸到胞质分裂期间收缩环的发育，其中微管和微丝系统之间存在相互作用。
