Department of Theoretical Physics, Helmholtz Centre Berlin for Materials and Energy, Berlin, Germany.
Biophys J. 2010 Apr 21;98(8):1571-81. doi: 10.1016/j.bpj.2009.12.4311.
We propose a mathematical model for simulating the leading-edge dynamics of a migrating cell from the interplay among elastic properties, architecture of the actin cytoskeleton, and the mechanics of the membrane. Our approach is based on the description of the length and attachment dynamics of actin filaments in the lamellipodium network. It is used to determine the total force exerted on the membrane at each position along the leading edge and at each time step. The model reproduces the marked state switches in protrusion morphodynamics found experimentally between epithelial cells in control conditions and cells expressing constitutively active Rac, a signaling molecule involved in the regulation of lamellipodium network assembly. The model also suggests a mechanistic explanation of experimental distortions in protrusion morphodynamics induced by deregulation of Arp2/3 and cofilin activity.
我们提出了一个数学模型，用于模拟从弹性性质、肌动蛋白细胞骨架结构和膜力学相互作用中迁移细胞的前缘动力学。我们的方法基于描述在片状伪足网络中肌动蛋白丝的长度和附着动力学。它用于确定在沿前缘的每个位置和每个时间步上作用在膜上的总力。该模型再现了在对照条件下上皮细胞和表达组成性激活 Rac 的细胞之间的实验中发现的突起形态动力学中的显著状态转换，Rac 是一种参与调节片状伪足网络组装的信号分子。该模型还提出了实验中突起形态动力学扭曲的机制解释，这些扭曲是由 Arp2/3 和丝切蛋白活性的失调引起的。
