Regulation of actin dynamics in rapidly moving cells: A quantitative analysis
Regulation of actin dynamics in rapidly moving cells: A quantitative analysis
复制标题
DOI：
10.1016/s0006-3495(02)73897-6
复制
发表时间：
2002-09-01
影响因子：
3.4
通讯作者：
Edelstein-Keshet, L
中科院分区：
文献类型：
--
作者：
Mogilner, A;Edelstein-Keshet, L
我们开发了一个数学模型，描述了与细胞运动性相关的突起肌动蛋白动力学的关键细节。该模型是基于树突状成核假说的lannellipodial突起的非肌肉细胞，如角膜细胞。我们考虑一组偏微分方程的扩散和反应的螯合肌动蛋白复合物，成核和生长的肌动蛋白丝的倒刺端的聚合，以及帽和解聚的细丝。突出的机械方面是基于弹性聚合棘轮机构。模型的输出是突出速度与推动膜的细丝倒钩末端的数量之间的关系。值得注意的是，这种关系有一个局部最大值：太多的倒刺末端耗尽了可用的单体库，太少不足以产生伸缩力，因此运动性在任何一个极端都是停滞的。我们的研究结果表明，要实现快速运动，一些调整参数影响肌动蛋白动力学必须在细胞中运行。
We develop a mathematical model that describes key details of actin dynamics in protrusion associated with cell motility. The model is based on the dendritic-nucleation hypothesis for lannellipodial protrusion in nonmuscle cells such as keratocytes. We consider a set of partial differential equations for diffusion and reactions of sequestered actin complexes, nucleation, and growth by polymerization of barbed ends of actin filaments, as well as capping and depolymerization of the filaments. The mechanical aspect of protrusion is based on an elastic polymerization ratchet mechanism. An output of the model is a relationship between the protrusion velocity and the number of filament barbed ends pushing the membrane. Significantly, this relationship has a local maximum: too many barbed ends deplete the available monomer pool, too few are insufficient to generate protrusive force, so motility is stalled at either extreme. Our results suggest that to achieve rapid motility, some tuning of parameters affecting actin dynamics must be operating in the cell.