Carlsson A E
Department of Physics, Washington University, Campus Box 1105, One Brookings Drive, St. Louis, MO. 63130, U.S.A.
New J Phys. 2011 Jul 1;13. doi: 10.1088/1367-2630/13/7/073009.
The mechanisms by which cytoskeletal flows and cell-substrate interactions interact to generate cell motion are explored using a simplified model of the cytoskeleton as a viscous gel containing active stresses. This model yields explicit general results relating cell speed and traction forces to the distributions of active stress and cell-substrate friction. It is found that 1) the cell velocity is given by a function that quantifies the asymmetry of the active-stress distribution, 2) gradients in cell-substrate friction can induce motion even when the active stresses are symmetrically distributed, 3) the traction-force dipole is enhanced by protrusive stresses near the cell edges or contractile stresses near the center of the cell, and 4) the cell velocity depends biphasically on the cell-substrate adhesion strength if active stress is enhanced by adhesion. Specific experimental tests of the calculated dependences are proposed.
利用一个简化的细胞骨架模型(将其视为含有主动应力的粘性凝胶),探究细胞骨架流动与细胞 - 基质相互作用相互影响以产生细胞运动的机制。该模型得出了将细胞速度和牵引力与主动应力分布及细胞 - 基质摩擦力相关联的明确通用结果。研究发现:1)细胞速度由一个量化主动应力分布不对称性的函数给出;2)即使主动应力对称分布,细胞 - 基质摩擦力的梯度也能诱导运动;3)细胞边缘附近的突出应力或细胞中心附近的收缩应力会增强牵引力偶极;4)如果主动应力因黏附作用而增强,细胞速度对细胞 - 基质黏附强度呈双相依赖。文中还提出了对计算得出的相关性进行具体实验测试的建议。