细胞迁移是多细胞生物发育的重要环节。尽管调控细胞迁移的信号和受体等关键因子已被发现，但是胞外信号如何通过膜上受体传递到微丝骨架上从而驱动细胞迁移还不清楚。前人的研究表明线虫的RhoG同源蛋白MIG-2在神经细胞迁移过程中发挥功能，但是其下游效应因子未知。我们的前期工作表明微丝结合蛋白Anillin富集在迁移细胞的前导端，稳定微丝网络，调控Q神经前体细胞迁移，而且发现Anillin结合MIG-2。我们推测Anillin可能是连接RhoG信号通路和微丝骨架之间的关键因子。我们的前期工作还表明Anillin的结合蛋白Septin也分布在迁移细胞的前导端，调控微丝骨架和细胞迁移。本课题将深入研究RhoG信号如何通过Anillin和Septin的传递，调控细胞前导端的微丝骨架稳定性促进细胞迁移。预期的成果将有助于更好的理解细胞迁移的机制，为相关疾病的发生及治疗提供新的思路。

Cell migration is essential for metazoan development. Despite the wealth of information about guidance cues, receptors and the machinery that powers motility, our understanding of the connection between receptor activation and the actin cytoskeleton remains elusive. Previous studies reported that the C. elegans RhoG homolog, MIG-2, is required for neuronal migration, but its downstream effector is largely unexplored. Our preliminary results showed that an actin-binding protein Anillin regulates cell migration by stabilizing the F-actin network at the leading edge of the migrating cell. Our results also demonstrated that Anillin can bind to RhoG/MIG-2 in vitro, indicating that Anillin may provide a previously unknown connection between RhoG/MIG-2 and F-actin network. Moreover, we found that an Anillin-binding protein, Septin, also can regulate Q cell migration. We propose to further address whether Anillin and Sepitn bind to RhoG and how they regulate the actin cytoskeleton during neuronal migration. We expect that our study will provide a novel mechanism for stabilizing actin filaments at the leading edge during neuronal migration, and shed light on the cell migration related diseases.