Stowers Institute for Medical Research, Kansas City, Missouri, USA.
Biophys J. 2013 Aug 6;105(3):547-54. doi: 10.1016/j.bpj.2013.06.033.
One of the unresolved questions in the field of cell division is how the actomyosin cytoskeleton remains structurally organized while generating the contractile force to divide one cell into two. In analogy to the actomyosin-based force production mechanism in striated muscle, it was originally proposed that contractile stress in the actomyosin ring is generated via a sliding filament mechanism within an organized sarcomere-like array. However, over the last 30 years, ultrastructural and functional studies have noted important distinctions between cytokinetic structures in dividing cells and muscle sarcomeres. Myosin-II motor activity is not always required, and there is evidence that actin depolymerization contributes to contraction. In this Review, the architecture and contractile dynamics of the actomyosin ring at the cell division plane will be discussed. We will report the interdisciplinary advances in the field as well as their integration into a mechanistic understanding of contraction in cell division and in other biological processes that rely on an actomyosin-based force-generating system.
细胞分裂领域中尚未解决的问题之一是,肌动球蛋白细胞骨架如何在产生将一个细胞分裂成两个的收缩力的同时保持结构组织。与横纹肌中的基于肌动球蛋白的力产生机制类似,最初提出的是,肌球蛋白环中的收缩应力是通过在组织类似于肌节的阵列内的滑动细丝机制产生的。然而,在过去的 30 年中,超微结构和功能研究已经注意到分裂细胞中的细胞分裂结构与肌肉肌节之间的重要区别。肌球蛋白-II 运动活性并不总是必需的,并且有证据表明肌动蛋白解聚有助于收缩。在这篇综述中,将讨论细胞分裂平面处的肌动球蛋白环的结构和收缩动力学。我们将报告该领域的跨学科进展,并将其整合到对细胞分裂和其他依赖肌动球蛋白产生力系统的生物学过程中的收缩的机械理解中。