Microtubule depolymerization induces stress fibers, focal adhesions, and DNA synthesis via the GTP-binding protein rho
Microtubule depolymerization induces stress fibers, focal adhesions, and DNA synthesis via the GTP-binding protein rho
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DOI：
10.3109/15419069809040295
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发表时间：
1998-01-01
期刊：
影响因子：
--
通讯作者：
Burridge, K
中科院分区：
文献类型：
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作者：
Liu, BP;Chrzanowska-Wodnicka, M;Burridge, K
微管解聚具有多种后果，包括肌动蛋白应力纤维和粘着斑组装，增加酪氨酸磷酸化和DNA合成。血清或溶血磷脂酸等试剂诱导的类似效应先前已显示由GTP结合蛋白Rho介导。我们已经研究了微管解聚的影响是否同样由Rho介导，并表明它们被特定的Rho抑制剂C3转移酶阻断。由于微管解聚诱导这些作用在静止的细胞，其中Rho基本上是不活跃的，我们得出结论，微管解聚导致Rho的激活。响应微管解聚和随之而来的刺激收缩性的Rho的激活表明微管可以调节微丝功能在各种运动现象的机制。这些范围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。
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.