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How cells with diverse morphologies and cytoskeletal architectures modulatetheir mechanical behaviors to drive robust collective motion within tissues ispoorly understood. During wound repair within epithelial monolayers in vitro,cells coordinate the assembly of branched and bundled actin networks toregulate the total mechanical work produced by collective cell motion. Usingtraction force microscopy, we show that the balance of actin networkarchitectures optimizes the wound closure rate and the magnitude of themechanical work. These values are constrained by the effective power exerted bythe monolayer, which is conserved and independent of actin architectures. Usinga cell-based physical model, we show that the rate at which mechanical work isdone by the monolayer is limited by the transformation between actin networkarchitectures and differential regulation of cell-substrate friction. Theseresults and our proposed molecular mechanisms provide a robust quantitativemodel for how cells collectively coordinate their non-equilibrium behaviors todynamically regulate tissue-scale mechanical output.

Epithelial Wound Healing Coordinates Distinct Actin Network Architectures to Conserve Mechanical Work and Balance Power