细胞迁移
电池极性
细胞粘附
丝状体
CDC42型
细胞骨架
细胞结
细胞
RAC1
肌动蛋白细胞骨架
形态发生
焦点粘着
粘附
作者
Masayuki Ozawa,Sylvain Hiver,Toshiyoshi Yamamoto,Tatsuo Shibata,Srigokul Upadhyayula,Yuko Mimori-Kiyosue,Masatoshi Takeichi
标识
DOI:10.1083/jcb.202006196
摘要
Collective migration of epithelial cells plays crucial roles in various biological processes such as cancer invasion. In migrating epithelial sheets, leader cells form lamellipodia to advance, and follower cells also form similar motile apparatus at cell–cell boundaries, which are called cryptic lamellipodia (c-lamellipodia). Using adenocarcinoma-derived epithelial cells, we investigated how c-lamellipodia form and found that they sporadically grew from around E-cadherin–based adherens junctions (AJs). WAVE and Arp2/3 complexes were localized along the AJs, and silencing them not only interfered with c-lamellipodia formation but also prevented follower cells from trailing the leaders. Disruption of AJs by removing αE-catenin resulted in uncontrolled c-lamellipodia growth, and this was brought about by myosin II activation and the resultant contraction of AJ-associated actomyosin cables. Additional observations indicated that c-lamellipodia tended to grow at mechanically weak sites of the junction. We conclude that AJs not only tie cells together but also support c-lamellipodia formation by recruiting actin regulators, enabling epithelial cells to undergo ordered collective migration.
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