组织液化和集体运动在调节胚胎形态发生、伤口愈合和肿瘤转移过程中起着关键作用。这些过程经常需要组织中的每个细胞成分通过定向扩展的薄片状细胞突起来协调其迁移活动和定向运动，该过程由RAC1活性促进。虽然在个体迁移细胞或入侵或伤口愈合过程中的领导者细胞中上游RAC1调控因子已经很好地被表征，但RAC1在跟随细胞中的调控方式仍然未知。在这里，我们确定了一个在模型组织单层中以平面极化方式空间限制RAC1活性的MYO6-DOCK7轴的重要性。MYO6-DOCK7轴特异地控制了必需推动组织液化和合作模式运动的隐蔽薄片状细胞突起的扩展，这些细胞集体在其他情况下都是固态和静止的。版权所有 © 2023 作者。由Elsevier Inc.出版。保留所有权利。

Tissue fluidification and collective motility are pivotal in regulating embryonic morphogenesis, wound healing, and tumor metastasis. These processes frequently require that each cell constituent of a tissue coordinates its migration activity and directed motion through the oriented extension of lamellipodium cell protrusions, promoted by RAC1 activity. While the upstream RAC1 regulators in individual migratory cells or leader cells during invasion or wound healing are well characterized, how RAC1 is controlled in follower cells remains unknown. Here, we identify a MYO6-DOCK7 axis essential for spatially restricting RAC1 activity in a planar polarized fashion in model tissue monolayers. The MYO6-DOCK7 axis specifically controls the extension of cryptic lamellipodia required to drive tissue fluidification and cooperative-mode motion in otherwise solid and static carcinoma cell collectives.Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.