Defects in the maintenance of intercellular junctions are associated with loss of epithelial barrier function and consequent pathological conditions, including invasive cancers. Epithelial integrity is dependent on actomyosin bundles at adherens junctions, but the origin of these junctional bundles is incompletely understood. Here we show that peripheral actomyosin bundles can be generated from a specific actin stress fiber subtype, transverse arcs, through their lateral fusion at cell-cell contacts. Importantly, we find that assembly and maintenance of peripheral actomyosin bundles are dependent on the mechanosensitive CaMKK2/AMPK signaling pathway and that inhibition of this route leads to disruption of tension-maintaining actomyosin bundles and re-growth of stress fiber precursors. This results in redistribution of cellular forces, defects in monolayer integrity, and loss of epithelial identity. These data provide evidence that the mechanosensitive CaMKK2/AMPK pathway is critical for the maintenance of peripheral actomyosin bundles and thus dictates cell-cell junctions through cellular force distribution.

维持细胞间连接的缺陷与上皮屏障功能的丧失和随之而来的病理状况（包括浸润性癌症）有关。上皮的完整性取决于粘附连接处的肌动球蛋白束，但这些连接束的起源尚不完全清楚。在这里，我们显示外围肌动蛋白束可以通过特定的肌动蛋白应激纤维亚型，横向弧，通过它们在细胞-细胞接触处的横向融合而产生。重要的是，我们发现外围肌动球蛋白束的组装和维护取决于机械敏感的CaMKK2 / AMPK信号传导途径，并且对该途径的抑制导致维持张力的肌动球蛋白束的破坏和应力纤维前体的重新生长。这导致细胞力的重新分配，单层完整性方面的缺陷，以及上皮身份的丧失。这些数据提供了机械敏感性CaMKK2 / AMPK途径对于维持周边放线菌素束至关重要，因此通过细胞力分布决定了细胞间的连接。