Injury compromises epithelial tissue biomechanics by breaking the mechanical coherence between its constituent cells, but how tissues efficiently remove damaged cells remains incompletely understood. In this talk I will focus on the role that mechanochemical control of epithelial junctional biomechanics plays in tissue repair. We found that the Src tyrosine kinase is activated in cells up to 3 cell diameters from the site of injury in confluent epithelial monolayers. This activation (at ~10 min after injury) is required for the collective rearrangement of these cells that leads to the clearance (extrusion) of damaged cells. We found that the activation of junctional Src signalling depends upon the relaxation of mechanical tension in the junctions. Further, we identified an increase in junctional actin turnover, mediated by cofilin-1, as a key step that allowed junctional relaxation to activate Src. We pursued this by developing a computational model of epithelial cells to describe the process of injury. In our model, injury caused a local relaxation of the monolayer up to 4 cell diameters beyond the point of injury that correlated well with Src activation spatial-scales and which we confirmed experimentally using laser nanoscissors. Introducing cofilin-dependent Src mechanosensing into the model increases the efficiency and speed of extrusion. Extrusion in the model was slowed when mechanochemical signaling was removed, which exactly matched observations in injured monolayers treated with Src inhibitors. Thus, our experimental and in silico results showed that the mechanochemical control of cell signalling plays a key role in preserving tissue integrity by determining the pattern of collective responses that favours the extrusion of damaged cells.