Actin crosslinking is required for force sensing at tricellular junctions.

ABSTRACT: Mechanical forces are essential for tissue morphogenesis, but risk causing ruptures that could compromise tissue function. In epithelial tissues, adherens junctions withstand the forces that drive morphogenesis by recruiting proteins that stabilize cell adhesion and reinforce connections to the actin cytoskeleton under tension. However, how junctional actin networks respond to forces in vivo is not well understood. Here we show that the actin crosslinker Fimbrin is recruited to tricellular junctions under tension and plays a central role in amplifying actomyosin contractility and stabilizing cell adhesion. Loss of Fimbrin results in a failure to reorganize actin under tension and an inability to enhance myosin-II activity and recruit junction-stabilizing proteins in response to forc

SUBMITTER: Taneja N 

PROVIDER: S-EPMC11888364 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature