Motor activity of nonmuscle myosin 2A is a key component of bipolar filament turnover in cells

Cell contractility plays numerous essential roles in a healthy organism, while its malfunctioning can lead to disease. The ubiquitous actin-dependent motors of the nonmuscle myosin 2 (NM2) family, which includes NM2A and NM2B, are chiefly responsible for cell contractility because of their ability to polymerize into bipolar filaments. Polymerization/depolymerization of NM2 filaments allows cells to quickly reorganize their contractile system according to constantly changing shapes and positions of nonmuscle cells. Bipolar filament depolymerization is known to depend on the C-terminal features of the NM2A heavy chain. Here, we show that the motor activity of NM2A is another key component of NM2As depolymerization mechanism, which cooperates with tail-dependent mechanisms to facilitate NM2A turnover in cells and, through copolymerization with NM2B, to reorganize and dynamize NM2B in trans, thus generating a proper intracellular NM2A/NM2B distribution needed for efficient cell migration. Together, we show that NM2A motor activity is a key component of the bipolar filament depolymerization mechanism.