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