Cell wound repair requires the coordinated action of linear and branched actin nucleation factors

Abstract

ABSTRACTCells are subjected to a barrage of daily insults that often lead to its cortex being ripped open and requiring immediate repair. An important component of the cell’ s repair response is the formation of an actomyosin ring at the wound periphery to mediate its closure. Inhibition of linear actin nucleation factors and myosin result in a disrupted contractile apparatus and delayed wound closure. Here we show that branched actin nucleators function as a scaffold to assemble and maintain this contractile actomyosin cable. Removing branched actin leads to the formation of smaller circular actin-myosin structures at the cell cortex and slow wound closure. Removing linear and branched actin results in failed wound closure. Surprisingly, removal of branched actin and myosin results in the formation of parallel linear actin filaments that undergo a chiral swirling movement to close the wound. These results provide insight into actin organization in contractile actomyosin rings and uncover a new mechanism of wound closure.SummaryHui et al. find that branched actin is required during cell wound repair to serve as a scaffold to anchor the contractile actomyosin cable at the wound periphery. Inhibition of branched actin and myosin results in parallel linear filaments that swirl to close the wound, uncovering a new mechanism for cell wound repair.