Laboratory Molecular Cell Biology and Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK.
Curr Opin Cell Biol. 2013 Oct;25(5):591-9. doi: 10.1016/j.ceb.2013.05.001. Epub 2013 Jun 11.
For decades, ever growing data on myosin II provides strong evidence that interaction of myosin-II-motor-domain with actin filaments within cells retracts the cell rear during actin-based cell migration. Now it is clear myosin II motor-activity is not the sole force involved. Alternative force-generating mechanisms within cells clearly also exist to power cell rear retraction during actin-based cell migration. Given that nematode sperm cells migrate without actin and without cytoskeletal motor proteins it is perhaps not surprising other types of force power cell rear retraction in actin-based systems. Here, cell rear retraction driven by actin filament depolymerisation, actin filament crosslinking, cell front protrusion and possibly apparent membrane tension and their importance relative to myosin II-motor-based contractility are discussed.
几十年来,越来越多的肌球蛋白 II 数据提供了强有力的证据,表明细胞内肌球蛋白 II-运动域与肌动蛋白丝的相互作用会在基于肌动蛋白的细胞迁移过程中缩回细胞后部。现在很明显,肌球蛋白 II 的运动活性并不是唯一涉及的力。细胞内显然还存在其他产生力的机制,以在基于肌动蛋白的细胞迁移过程中为细胞后部的缩回提供动力。鉴于线虫精子细胞在没有肌动蛋白和细胞骨架运动蛋白的情况下迁移,其他类型的力在基于肌动蛋白的系统中推动细胞后部的缩回也就不足为奇了。在这里,由肌动蛋白丝解聚、肌动蛋白丝交联、细胞前缘突出以及可能的明显膜张力驱动的细胞后部缩回及其相对于肌球蛋白 II 基于收缩的重要性进行了讨论。