Abstract
Repair of disruptions to the plasma membrane is an essential mechanism for maintenance of cellular homeostasis and integrity, a process that involves coordinated movement of intracellular vesicles to membrane injury sites for patch formation. We have previously identified MG53 as an essential component of the cell membrane repair machinery. In order for MG53 and intracellular vesicles to translocate to membrane injury sites, motor proteins must be involved. Here we show that non-muscle myosin type IIA (NM-IIA) interact with MG53 to regulate vesicle trafficking in both muscle and non-muscle cells. In cells that are deficient for NM-IIA expression, MG53 cannot translocate to acute injury sites, whereas rescue of NM-IIA expression in these cells can restore MG53-mediated membrane repair. Compromised cell membrane repair is observed in cells with RNAi-mediated knockdown of NM-IIA expression, or pharmacological interventions of NM-IIA motor function. Thus, our dada reveal NM-IIA as a key cytoskeletal motor that facilitates vesicle trafficking for MG53-mediated cell membrane repair.
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