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Nat Phys. 2019;15:696-705. doi: 10.1038/s41567-019-0485-9. Epub 2019 Apr 8.

Wound Healing Coordinates Actin Architectures to Regulate Mechanical Work.

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Department of Biomedical Engineering, Yale University, 55 Prospect Street, New Haven, Connecticut 06511, USA.
Systems Biology Institute, Yale University, 850 West Campus Drive, West Haven, Connecticut 06516, USA.
Department of Biomedical Engineering, University of Wisconsin-Madison, 1550 Engineering Drive, Madison, WI, 53706, USA.
Department of Physics and Astronomy, Institute for the Physics of Living Systems, University College London, Gower Street, London WC1E 6BT, UK.
Department of Physics, Yale University, 217 Prospect Street, New Haven, Connecticut 06511, USA.
Department of Molecular Genetics and Cell Biology, University of Chicago, 920 E. 58 St, Chicago, IL, 60637, USA.
Department of Physics, Northeastern University, 111 Dana Research Center, Boston, MA 02115, USA.


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 mechanisms provide a robust physical model for how cells collectively coordinate their non-equilibrium behaviors to dynamically regulate tissue-scale mechanical output.

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