LAUSR

Actomyosin (actin‐myosin II complex)‐mediated contractile forces are central to the generation of multifaceted uni‐ and multi‐cellular material properties and dynamics such as cell division, migration, and tissue morphogenesis. In the present article, we summarize our recent researches addressing molecular mechanisms that ensure actomyosin‐mediated directional cell–cell junction remodeling, either shortening or extension, driving cell rearrangement for epithelial morphogenesis. Genetic perturbation clarified two points concerning cell–cell junction remodeling: an inhibitory mechanism against negative feedback in which actomyosin contractile forces, which are well known to induce cell–cell junction shortening, can concomitantly alter actin dynamics, oppositely leading to perturbation of the shortening; and tricellular junctions as a point that organizes extension of new cell–cell junctions after shortening. These findings highlight the notion that cells develop underpinning mechanisms to transform the multi‐tasking property of actomyosin contractile forces into specific and proper cellular dynamics in space and time.