Within tissues, key cellular adaptations occur via mechanotransduction responses at cell–cell junctions. Adherens junctions (AJs) typically form between cells as a result of the binding of cadherin receptors of the same type (homotypic), and are linked to the force-propagating and -generating actomyosin cytoskeleton. Recent studies have found that AJs maintain monolayer integrity in dynamic tissues and drive collective cell behavior by converting into asymmetric remodeling entities. Here, we overview the molecular processes that may explain how asymmetric cell–cell junctions sense differences in cytoskeletal geometry between cells. We discuss the link between cadherin-complex dynamics and the actomyosin cytoskeleton at asymmetric cell–cell junctions. We then outline the role of Bin/Amphiphysin/Rvs (BAR) proteins, cytoplasmic regulators of endocytosis and cytoskeletal dynamics that sense force-induced membrane curvature, at AJs undergoing asymmetric remodeling. Lastly, we highlight the physiological importance of junctional asymmetry for epithelial and vascular tissue and discuss its potential role in disease.

在组织内，关键的细胞适应通过细胞间连接处的机械转导反应发生。粘附连接（AJs）通常是由于相同类型的钙粘着蛋白受体（同型）结合而在细胞之间形成的，并与力传播和产生的肌动球蛋白细胞骨架相连。最近的研究发现，AJ通过转化为不对称的重塑实体来维持动态组织中的单层完整性并驱动集体细胞行为。在这里，我们概述了可以解释不对称细胞间连接如何感测细胞之间细胞骨架几何结构差异的分子过程。我们讨论了钙粘蛋白复合动力学与不对称细胞间连接处的放线菌素细胞骨架之间的联系。然后，我们概述Bin / Amphiphysin / Rvs（BAR）蛋白的作用，进行不对称重塑的AJ的胞吞内吞和细胞骨架动力学的细胞质调节剂，可感应力诱导的膜曲率。最后，我们强调了交界不对称对上皮和血管组织的生理重要性，并讨论了其在疾病中的潜在作用。