Abstract
Closing gaps in cellular monolayers is a fundamental aspect of both morphogenesis and wound healing. This closure can be achieved through leader cell crawling or actomyosin-based contraction, depending on the size of the gap. Here, we focus on wounds whose closure is driven by interfacial instabilities, featuring both leader cell-driven fingers and actin-mediated contraction. Our proposed model predicts a positive correlation between the frequency of fingering and the overall speed of boundary closure. This fingering frequency is precisely regulated through the orchestration of cell density-driven pressure, cell-cell repulsions, and the initial curvature of the wound boundary. Our findings demonstrate an inverse correlation between fingering frequency and boundary curvatures, indicating a “self-control” mechanism for closure rates independent of the initial curvatures of the wound periphery. Notably, changes in curvature caused by fingering formation generate force that aids in the healing process.
Competing Interest Statement
The authors have declared no competing interest.