Department of Biological Physics, Eötvös University, 1117 Budapest, Pa´zma´ny P stny 1A, Hungary.
Cytoskeleton (Hoboken). 2011 Jun;68(6):325-39. doi: 10.1002/cm.20515.
We investigate the effect of myosin II inhibition on cell shape and nuclear motility in cultures of mouse radial glia-like neural progenitor and rat glioma C6 cells. Instead of reducing nucleokinesis, the myosin II inhibitor blebbistatin provokes an elongated bipolar morphology and increased nuclear motility in both cell types. When myosin II is active, time-resolved traction force measurements indicate a pulling force between the leading edge and the nucleus of C6 cells. In the absence of myosin II activity, traction forces during nucleokinesis are diminished below the sensitivity threshold of our assay. By visualizing the centrosome position in C6 cells with GFP-centrin, we show that in the presence or absence of myosin II activity, the nucleus tends to overtake or lag behind the centrosome, respectively. We interpret these findings with the help of a simple viscoelastic model of the cytoskeleton consisting active contractile and passive compressed elements.
我们研究了肌球蛋白 II 抑制对培养的鼠放射状胶质样神经祖细胞和大鼠神经胶质瘤 C6 细胞的细胞形状和核运动的影响。肌球蛋白 II 抑制剂 blebbistatin 并没有减少核分裂，反而引起两种细胞类型的拉长双极形态和核运动增加。当肌球蛋白 II 活跃时，时间分辨牵引力测量表明 C6 细胞的前缘和核之间存在拉力。在没有肌球蛋白 II 活性的情况下，核分裂过程中的牵引力减小到低于我们测定的灵敏度阈值。通过用 GFP 中心体可视化 C6 细胞中的中心体位置，我们表明，无论肌球蛋白 II 活性的存在与否，核往往会分别超过或落后于中心体。我们借助一个由活跃的收缩和被动压缩元件组成的简单粘弹性细胞骨架模型来解释这些发现。
