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Inhibition of myosin II triggers morphological transition and increased nuclear motility.

机译:抑制肌球蛋白II触发形态转型和核动动力增加。

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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.
机译:我们探讨了肌霉素II抑制对小鼠径向胶胶状神经祖细胞和大鼠胶质瘤C6细胞培养细胞形状和核动力的影响。 肌球蛋白II抑制剂Blebbistatis代替减少核因素,而是引起细长的双极形态并增加两种细胞类型的核动力障碍。 当肌球蛋白II是有效的,时间分辨的牵引力测量指示C6细胞的前缘和核之间的拉力。 在没有肌球蛋白II活性的情况下,核因素期间的牵引力降低低于我们测定的灵敏度阈值。 通过用GFP-Centrin可视化C6细胞中的中心体位置,我们表明在存在或不存在肌霉菌素II活性时,核趋于分别超过中心体延迟或滞后。 我们是借助于组成的细胞骨架的简单粘弹性模型来解释这些发现,包括有源收缩和被动压缩元件。

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