Zipkin I D, Kindt R M, Kenyon C J
Department of Biochemistry and Biophysics, University of California, San Francisco 94143-0554, USA.
Cell. 1997 Sep 5;90(5):883-94. doi: 10.1016/s0092-8674(00)80353-0.
Rho family GTPases are thought to regulate actin-dependent processes, but their functions in vivo are still poorly understood. We have investigated the function of a new, widely expressed Rho family member in C. elegans by analyzing mutations in the endogenous gene. Activated and null alleles all inhibit cell migration, demonstrating that this protein is required for cell migration in vivo. Only a small subset of the migrations inhibited by activating mutations are inhibited by null mutations, suggesting that considerable functional redundancy exists within this system. Our findings support this conclusion and show that mig-2 functions redundantly with another pathway to regulate nuclear migration. Surprisingly, activated alleles also cause misguided axon growth, suggesting that Rho family GTPases may couple guidance cues to process outgrowth.
Rho家族GTP酶被认为可调节肌动蛋白依赖性过程，但其在体内的功能仍知之甚少。我们通过分析线虫内源性基因中的突变，研究了一种新的、广泛表达的Rho家族成员的功能。激活型和无效等位基因均抑制细胞迁移，表明该蛋白是体内细胞迁移所必需的。激活型突变抑制的迁移中，只有一小部分被无效突变所抑制，这表明该系统内存在相当程度的功能冗余。我们的研究结果支持这一结论，并表明mig-2与另一条调节核迁移的途径存在功能冗余。令人惊讶的是，激活型等位基因还会导致轴突生长错误，这表明Rho家族GTP酶可能将导向线索与突起生长联系起来。
