為了理解細胞在基板上爬行的力學機制，本論文提出了一個一維理論模型。此模 型包含了肌凝蛋白的收縮力、細胞骨架的黏滯力、鍵結和基板的阻力以及細胞前 後端肌動蛋白絲聚合之間的交互作用。數值模擬本模型的結果顯示（1）肌凝蛋 白的收縮力（2）肌動蛋白絲的聚合速率在細胞前後端的不對稱性（3）鍵結分布 的不對稱性可以幫助細胞爬行。當細胞利用收縮力爬行時，其靜止狀態時流場分 布為零，肌凝蛋白與鍵結在細胞中均勻分布。當肌動蛋白絲的聚合加入模型中時， 其靜止狀態的流場為逆流分布，肌凝蛋白向中間聚集，鍵結分布靠近細胞兩端。 當細胞開始移動時，流場與肌凝蛋白的分布失去前後對稱性，細胞前端的鍵結密 度會因為突出(protrusion)而降低。當細胞移動的速度越快，鍵結分布的極值會 越來越靠近細胞中段，這是因為成熟的鍵結需要時間形成。;To understand how the intracellular mechanics affect the motion of a cell, we develop a one-dimensional model for cell migration on a solid substrate. This model includes contractile force from actomyosin network, viscous stress in the cytoskeleton, actin polymerization at the ends of the cell, drag force due to substrate and cell-substrate bonds. Our numerical solutions show that cell motility is facilitated by (i) active contractility of the actyomyosin gel, (ii) asymmetric actin polymerization at cell ends, and (iii) symmetry-breaking in the distribution of cell-substrate bonds. The flow field is zero everywhere in the rest state when the cell motility is facilitated only by active contractility. The corresponding bond density is uniform. The flow field becomes retrograde in the rest state when actin polymerization is included. The corresponding bond density has peaks close to the cell ends for catch bonds. When the cell starts to move, the flow drives the asymmetric distribution of myosin motors. The bond density at the leading end becomes lower due to protrusion. As the speed of the cell increases, bonds in the leading half of the cell move closer to the center because the slow growth of mature focal adhesion complexes.
