Underlying mechanisms that ensure actomyosin‐mediated directional remodeling of cell–cell contacts for multicellular movement

Abstract

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.