肌动蛋白
细胞骨架
伤口愈合
牵引(地质)
物理
牵引力
工作(物理)
机械生物学
单层
生物系统
纳米技术
生物物理学
机械
细胞生物学
细胞
材料科学
化学
生物
机械工程
工程类
热力学
免疫学
生物化学
作者
Visar Ajeti,A. Pasha Tabatabai,Andrew J. Fleszar,Michael F. Staddon,Daniel S. Seara,Cristian Suarez,Muhammad Sulaiman Yousafzai,Dapeng Bi,David R. Kovar,Shiladitya Banerjee,Michael P. Murrell
出处
期刊:Nature Physics
[Springer Nature]
日期:2019-04-08
卷期号:15 (7): 696-705
被引量:61
标识
DOI:10.1038/s41567-019-0485-9
摘要
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. When a wound heals, different types of branched and bundled actin structure form, each designed to perform a specific function. Experiments and theory now suggest that the actin architecture depends on the stiffness of the cell’s surroundings.
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