Rac1 and Cdc42 capture microtubules through IQGAP1 and CLIP-170
Rac1 and Cdc42 capture microtubules through IQGAP1 and CLIP-170
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DOI：
10.1016/s0092-8674(02)00800-0
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发表时间：
2002-06-28
期刊：
影响因子：
64.5
通讯作者：
Kaibuchi, K
中科院分区：
文献类型：
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作者：
Fukata, M;Watanabe, T;Kaibuchi, K
微管与特定皮质区域的连接对于细胞极化至关重要。CLIP - 170与微管的生长末端结合，并在定向中起关键作用。我们发现IQGAP1（Rac1和Cdc42的效应物）与CLIP - 170相互作用。在非洲绿猴肾成纤维细胞中，IQGAP1定位于极化的前沿。包含CLIP - 170结合区域的IQ - GAP1羧基末端片段的表达使绿色荧光蛋白 - CLIP - 170从微管末端移位，并改变微管阵列。活化的Rac1/Cdc42、IQGAP1和CLIP - 170形成一个三元复合物。此外，表达在Rac1/Cdc42结合方面有缺陷的IQGAP1突变体可诱导多个前沿。这些结果表明，Rac1/Cdc42标记了IQGAP1和CLIP - 170复合物所靶向的特定皮质位点，从而导致极化的微管阵列和细胞极化。
Linkage of microtubules to special cortical regions is essential for cell polarization. CLIP-170 binds to the growing ends of microtubules and plays pivotal roles in orientation. We have found that IQGAP1, an effector of Rac1 and Cdc42, interacts with CLIP-170. In Vero fibroblasts, IQGAP1 localizes at the polarized leading edge. Expression of carboxy-terminal fragment of 1Q-GAP1, which includes the CLIP-170 binding region, delocalizes GFP-CLIP-170 from the tips of microtubules and alters the microtubule array. Activated Rac1/Cdc42, IQGAP1, and CLIP-170 form a tripartite complex. Furthermore, expression of an IQGAP1 mutant defective in Rac1/Cdc42 binding induces multiple leading edges. These results indicate that Rac1/Cdc42 marks special cortical spots where the IQGAP1 and CLIP-170 complex is targeted, leading to a polarized microtubule array and cell polarization.