Cells coordinate their movements during embryogenesis and tissue repair through the formation of multicellular cytoskeletal networks. In embryonic wound repair, actin and the motor protein non-muscle myosin II polarise in the cells adjacent to the lesion site. This polarisation leads to the formation of a supracellular actin cable around the lesion, which serves as a contracting purse string to coordinate migration of those cells next to the wound. How the dynamics of a motor protein, such as non-muscle myosin II, are regulated during wound repair is poorly understood. In their Short Report (p. 689), Rodrigo Fernandez-Gonzalez and colleagues now address myosin dynamics by using fluorescence recovery after photobleaching (FRAP) in Drosophila embryos. They demonstrate that – compared to turnover of epidermal actin cables with lower levels of contractility – turnover of myosin is reduced as purse strings contract at wounds. The authors then confirm in laser ablation experiments that tension at the purse string increases and is associated with reduced myosin turnover as wound closure progresses. Further, the mechanical tension at the purse string is necessary and sufficient to stabilise and maintain myosin at the wound edge. Indeed, the motor activity of myosin is required both for its stabilisation around the wound and for rapid wound closure. This work, thus, establishes a link between mechanical forces and the regulation of myosin dynamics in embryonic wound closure.