期刊
NATURE PHYSICS
卷 15, 期 7, 页码 696-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41567-019-0485-9
关键词
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资金
- ARO MURI [W911NF-14-1-0403]
- National Science Foundation (NSF) Fellowship [DGE1122492]
- NIH [RO1 GM126256, U54 CA209992]
- Yale Endowed Fund
- UK Engineering and Physical Sciences Research Council (EPSRC) PhD studentship at University College London (UCL)
- Royal Society Tata University Research Fellowship [URF/R1/180187]
- Strategic Fellowship at UCL
- Human Frontiers Science Program (HFSP) [RGY0073/2018]
- [CMMI-1525316]
How cells with diverse morphologies and cytoskeletal architectures modulate their mechanical behaviours 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 behaviours to dynamically regulate tissue-scale mechanical output.
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