Kurzawa Laetitia, Vianay Benoit, Senger Fabrice, Vignaud Timothée, Blanchoin Laurent, Théry Manuel
CytoMorpho Lab, Biosciences and Biotechnology Institute of Grenoble, UMR5168, Université Grenoble-Alpes, CEA, CNRS, INRA, 38054 Grenoble, France.
Université Paris Diderot, INSERM, CEA, CytoMorpho Lab, Hôpital Saint Louis, Institut Universitaire d'Hematologie, UMRS1160, 75010 Paris, France.
Mol Biol Cell. 2017 Jul 7;28(14):1825-1832. doi: 10.1091/mbc.E16-09-0672.
Mechanical forces are key regulators of cell and tissue physiology. The basic molecular mechanism of fiber contraction by the sliding of actin filament upon myosin leading to conformational change has been known for decades. The regulation of force generation at the level of the cell, however, is still far from elucidated. Indeed, the magnitude of cell traction forces on the underlying extracellular matrix in culture is almost impossible to predict or experimentally control. The considerable variability in measurements of cell-traction forces indicates that they may not be the optimal readout to properly characterize cell contractile state and that a significant part of the contractile energy is not transferred to cell anchorage but instead is involved in actin network dynamics. Here we discuss the experimental, numerical, and biological parameters that may be responsible for the variability in traction force production. We argue that limiting these sources of variability and investigating the dissipation of mechanical work that occurs with structural rearrangements and the disengagement of force transmission is key for further understanding of cell mechanics.
机械力是细胞和组织生理学的关键调节因子。几十年来，人们已经知道肌动蛋白丝在肌球蛋白上滑动导致构象变化从而引起纤维收缩的基本分子机制。然而，在细胞水平上力产生的调节仍远未阐明。实际上，培养中细胞对其下方细胞外基质的牵引力大小几乎无法预测或通过实验控制。细胞牵引力测量结果的显著差异表明，它们可能不是正确表征细胞收缩状态的最佳读数，并且收缩能量的很大一部分并未转移到细胞锚定上，而是参与了肌动蛋白网络动力学。在这里，我们讨论可能导致牵引力产生差异的实验、数值和生物学参数。我们认为，限制这些差异来源并研究结构重排和力传递脱离时发生的机械功耗散对于进一步理解细胞力学至关重要。
