Cytoskeletal cross-linking and bundling in motor-independent contraction.-猫眼课题宝

DOI：

10.1016/j.cub.2010.07.004

发表时间：

2010-08-10

期刊：

CURRENT BIOLOGY

影响因子：

9.2

通讯作者：

中科院分区：

生物学1区

文献类型：

作者：

Sun, Sean X.;Walcott, Sam;Wolgemuth, Charles W.

来源链接：

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3633214/?report=classic

真核细胞和原核细胞使用细胞骨架蛋白来调节和修饰细胞形状。在胞质分裂或真核细胞爬行过程中，细胞内产生收缩力，分别收缩分裂部位或牵引细胞后部向前。在许多情况下，这些力被归因于分子马达的活动，如肌球蛋白II，通过拉动肌动蛋白丝，可以产生肌动蛋白细胞骨架的收缩。然而，原核分裂是由微管蛋白样蛋白FtsZ驱动的，似乎不需要额外的分子马达来收缩分裂位点。同样，盘基网柄藻和酿酒酵母可以在无马达条件下进行胞质分裂。此外，当肌球蛋白被抑制或缺乏时，许多爬行细胞可以移位。在这篇综述中，我们指出了另一种力的产生机制，可以在驱动这些过程中发挥重要作用，在真核生物和原核生物。这一机制是通过交联和捆绑蛋白质介导的，这些蛋白质在细胞骨架丝之间形成有效的相互作用。最近在这方面的一些研究进行了审查，并解释了这种力产生机制的物理基础。

Eukaryotic and prokaryotic cells use cytoskeletal proteins to regulate and modify cell shape. During cytokinesis or eukaryotic cell crawling, contractile forces are generated inside the cell to constrict the division site or to haul the rear of the cell forward, respectively. In many cases, these forces have been attributed to the activity of molecular motors, such as myosin II, which, by pulling on actin filaments, can produce contraction of the actin cytoskeleton. However, prokaryotic division is driven by the tubulin-like protein FtsZ and does not seem to require additional molecular motors to constrict the division site. Likewise, Dictyostelium discoideum and Saccharomyces cerevisiae can perform cytokinesis under motor-free conditions. In addition, many crawling cells can translocate when myosin is inhibited or absent. In this review, we point out another force-generation mechanism that can play a significant role in driving these processes in eukaryotes and prokaryotes. This mechanism is mediated by cross-linking and bundling proteins that form effective interactions between cytoskeletal filaments. Some recent studies in this area are reviewed and the physical underpinnings of this force-generation mechanism are explained.