Cell：细胞运动受生物力学过程调节
细胞运动依赖于周期性的边缘凸起(edge protrusion)、粘着和恢复实现。但这些究竟是受生物化学还是生物力学过程调节的，一直是未解之谜。
来自美国哥伦比亚大学和法国波尔多二大学（Université Bordeaux 2）等科研机构的研究人员发现，myosin II牵引lamellipodial肌动蛋白网络（lamellipodial actin network）的后方向上弯曲、边缘收回和形成新的粘着位点。然后，lamellipodial肌动蛋白网络从边缘分开，围绕肌浆球蛋白（myosin）浓缩。当lamellipodial肌动蛋白从前端开始再生时，突起恢复并向后端扩展，直达新组装的myosin，开始下一轮运动。
Evanescence和电镜实验结果显示，粘着力不足时向上弯曲会形成纹状缘（ruffle）。相关荧光和电镜实验显示，新生的lamellipodial会在lamellum上形成一个粘着的、可分离的肌动蛋白层。因此，周期性的肌动蛋白聚合建立了一个机械的连接，lamellipodium将myosin马达与支持位点的起始联系起来，提示驱动力的主要功能是由一个生物力学过程调节的。
Lamellipodial Actin Mechanically Links Myosin Activity with Adhesion-Site Formation
Grégory Giannone,1,2,6 Benjamin J. Dubin-Thaler,1,6 Olivier Rossier,1 Yunfei Cai,1 Oleg Chaga,3 Guoying Jiang,1 William Beaver,4 Hans-Günther Döbereiner,1 Yoav Freund,4 Gary Borisy,3 and Michael P. Sheetz1,5,
Cell motility proceeds by cycles of edge protrusion, adhesion, and retraction. Whether these functions are coordinated by biochemical or biomechanical processes is unknown. We find that myosin II pulls the rear of the lamellipodial actin network, causing upward bending, edge retraction, and initiation of new adhesion sites. The network then separates from the edge and condenses over the myosin. Protrusion resumes as lamellipodial actin regenerates from the front and extends rearward until it reaches newly assembled myosin, initiating the next cycle. Upward bending, observed by evanescence and electron microscopy, results in ruffle formation when adhesion strength is low. Correlative fluorescence and electron microscopy shows that the regenerating lamellipodium forms a cohesive, separable layer of actin above the lamellum. Thus, actin polymerization periodically builds a mechanical link, the lamellipodium, connecting myosin motors with the initiation of adhesion sites, suggesting that the major functions driving motility are coordinated by a biomechanical process.
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