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首页> 外文期刊>Neuron >Myosin II motors and F-actin dynamics drive the coordinated movement of the centrosome and soma during CNS glial-guided neuronal migration.
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Myosin II motors and F-actin dynamics drive the coordinated movement of the centrosome and soma during CNS glial-guided neuronal migration.

机译:在中枢神经系统神经胶质引导的神经元迁移过程中,肌球蛋白II马达和F-肌动蛋白动力学驱动着中心体和躯体的协调运动。

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摘要

Lamination of cortical regions of the vertebrate brain depends on glial-guided neuronal migration. The conserved polarity protein Par6alpha localizes to the centrosome and coordinates forward movement of the centrosome and soma in migrating neurons. The cytoskeletal components that produce this unique form of cell polarity and their relationship to polarity signaling cascades are unknown. We show that F-actin and Myosin II motors are enriched in the neuronal leading process and that Myosin II activity is necessary for leading process actin dynamics. Inhibition of Myosin II decreased the speed of centrosome and somal movement, whereas Myosin II activation increased coordinated movement. Ectopic expression or silencing of Par6alpha inhibited Myosin II motors by decreasing Myosin light-chain phosphorylation. These findings suggest leading-process Myosin II may function to "pull" the centrosome and soma forward during glial-guided migration by a mechanism involving the conserved polarity protein Par6alpha.
机译:脊椎动物大脑皮质区域的层压取决于神经胶质引导的神经元迁移。保守的极性蛋白Par6alpha定位于中心体并协调中心体和体在迁移神经元中的向前运动。产生这种细胞极性独特形式的细胞骨架成分及其与极性信号级联反应的关系尚不清楚。我们显示F-肌动蛋白和肌球蛋白II电机丰富了神经元的主导过程,而肌球蛋白II活性对于主导过程肌动蛋白动力学是必要的。抑制肌球蛋白II降低了中心体和体细胞运动的速度,而肌球蛋白II的激活增加了协调运动。 Par6alpha的异位表达或沉默通过减少肌球蛋白轻链磷酸化抑制肌球蛋白II运动。这些发现表明,引导过程的肌球蛋白II可能通过涉及保守极性蛋白Par6alpha的机制在神经胶质引导的迁移过程中“拉”中心体和躯体向前。

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