Department of Functional Molecular Biology, Graduate School of Medicine, Yamaguchi University, Yamaguchi, Japan; Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh.
Department of Functional Molecular Biology, Graduate School of Medicine, Yamaguchi University, Yamaguchi, Japan.
Eur J Cell Biol. 2017 Sep;96(6):515-528. doi: 10.1016/j.ejcb.2017.06.004. Epub 2017 Jun 12.
Cytokinesis is the final stage of cell division. Dictyostelium cells have multiple modes of cytokinesis, including cytokinesis A, B and C. Cytokinesis A is a conventional mode, which depends on myosin II in the contractile ring. Myosin II null cells divide depending on substratum-attachment (cytokinesis B) or in a multi-polar fashion independent of the cell cycle (cytokinesis C). We investigated the traction stress exerted by dividing cells in the three different modes using traction force microscopy. In all cases, the traction forces were directed inward from both poles. Interestingly, the traction stress of cytokinesis A was the smallest of the three modes. Latrunculin B, an inhibitor of actin polymerization, completely diminished the traction stress of dividing cells, but blebbistatin, an inhibitor of myosin II ATPase, increased the traction stress. Myosin II is proposed to contribute to the detachment of cell body from the substratum. When the cell-substratum attachment was artificially strengthened by a poly-lysine coating, wild type cells increased their traction stress in contrast to myosin II null and other cytokinesis-deficient mutant cells, which suggests that wild type cells may increase their own power to conduct their cytokinesis. The cytokinesis-deficient mutants frequently divided unequally, whereas wild type cells divided equally. A traction stress imbalance between two daughter halves was correlated with cytokinesis failure. We discuss the regulation of cell shape changes during cell division through mechanosensing.
细胞分裂是细胞分裂的最后一个阶段。粘菌细胞有多种细胞分裂方式,包括细胞分裂 A、B 和 C。细胞分裂 A 是一种常规的方式,它依赖于收缩环中的肌球蛋白 II。肌球蛋白 II 缺失的细胞根据基质附着(细胞分裂 B)或在与细胞周期无关的多极方式(细胞分裂 C)进行分裂。我们使用牵引力显微镜研究了这三种不同模式下分裂细胞施加的牵引力。在所有情况下,牵引力都是从两极向内指向的。有趣的是,细胞分裂 A 的牵引力是三种模式中最小的。肌动蛋白聚合抑制剂 Latrunculin B 完全消除了分裂细胞的牵引力,但肌球蛋白 II ATP 酶抑制剂 Blebbistatin 增加了牵引力。肌球蛋白 II 被认为有助于细胞本体与基质的分离。当通过聚赖氨酸涂层人为地增强细胞-基质附着时,与肌球蛋白 II 缺失和其他细胞分裂缺陷突变体细胞相比,野生型细胞增加了它们的牵引力,这表明野生型细胞可能会增加它们自己进行细胞分裂的能力。细胞分裂缺陷突变体经常不均等地分裂,而野生型细胞则均等分裂。两个子细胞之间的牵引力不平衡与细胞分裂失败有关。我们讨论了通过机械感知来调节细胞分裂过程中的细胞形状变化。