Initiation of epithelial wound closure by an active instability at the purse string.

The ability of biological systems to withstand and recover from various disruptions, such as spontaneous genetic mutations and environmental damage, largely relies on intricate feedback mechanisms. We theoretically study the mechanical response of an epithelial tissue facing damage in the form of a circular wound. Our model describes a feedback loop between the generation of active forces in the actomyosin and tissue mechanics, described by the vertex model. While the exact dynamics of wound closure may be influenced by several biophysical mechanisms that interplay in a nontrivial way, our findings suggest that the closure may initiate as an active instability, triggered by a reduced myosin turnover rate at the wound's perimeter. We explore the interplay between myosin dynamics and the elastic properties of the tissue, elucidating their collective role in determining a wound's loss of stability, leading to the initiation of the closure process.