The actin cytoskeleton is involved in the regulation of cell morphology and migration. Wiskott-Aldrich Syndrome proteins (WASPs) play an important role in controlling actin polymerization by activating the Arp2/3 complex. The present study investigated the roles of WasC, one of the 3 WASPs in Dictyostelium, in cellular processes. Cells lacking WasC displayed strong cell adhesion and approximately 1.5-fold increase in F-actin levels as compared to the wild-type cells. Loss of wasC caused defects in phagocytosis and decreased the migration speed in chemoattractant-mediated cell migration but did not affect directionality. WasC was localized to the protruding region in migrating cells and, transiently and rapidly translocated to the cell cortex in response to chemoattractant stimulation, in an F-actin dependent manner. Our results suggest that WasC is involved in cell adhesion and migration by regulating F-actin polymerization at the leading edge of migrating cells, probably as a negative regulator. The increased strength of adhesion in wasC null cells is likely to decrease the migration speed but not the directionality

中文翻译：

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WasC是WASP家族的一种蛋白质，它通过调节Dictyostelium中的F-肌动蛋白聚合来参与细胞粘附和迁移。

肌动蛋白细胞骨架参与细胞形态和迁移的调节。Wiskott-Aldrich综合征蛋白（WASP）通过激活Arp2 / 3复合物在控制肌动蛋白聚合中起重要作用。本研究调查了Dictyostelium中3种WASP之一WasC的作用，在细胞过程中。与野生型细胞相比，缺乏WasC的细胞表现出强大的细胞粘附性，F-肌动蛋白水平提高约1.5倍。wasC的损失会导致吞噬作用的缺陷，并降低趋化因子介导的细胞迁移中的迁移速度，但不会影响方向性。WasC定位于迁移细胞中的突出区域，并以依赖于F-肌动蛋白的方式响应化学趋化刺激而迅速而迅速地转移至细胞皮层。我们的结果表明，WasC通过调节迁移细胞前沿的F-肌动蛋白聚合而参与细胞黏附和迁移，可能是作为负调节剂。wasC null细胞中粘附强度的增加可能会降低迁移速度，但不会降低方向性