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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Rac1 regulates neuronal polarization through the WAVE complex.
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Rac1 regulates neuronal polarization through the WAVE complex.

机译：RAC1通过波复合物调节神经元极化。

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摘要

Neuronal migration and axon growth, key events during neuronal development, require distinct changes in the cytoskeleton. Although many molecular regulators of polarity have been identified and characterized, relatively little is known about their physiological role in this process. To study the physiological function of Rac1 in neuronal development, we have generated a conditional knock-out mouse, in which Rac1 is ablated in the whole brain. Rac1-deficient cerebellar granule neurons, which do not express other Rac isoforms, showed impaired neuronal migration and axon formation both in vivo and in vitro. In addition, Rac1 ablation disrupts lamellipodia formation in growth cones. The analysis of Rac1 effectors revealed the absence of the Wiskott-Aldrich syndrome protein (WASP) family verprolin-homologous protein (WAVE) complex from the plasma membrane of knock-out growth cones. Loss of WAVE function inhibited axon growth, whereas overexpression of a membrane-tethered WAVE mutant partially rescued axon growth in Rac1-knock-out neurons. In addition, pharmacological inhibition of the WAVE complex effector Arp2/3 also reduced axon growth. We propose that Rac1 recruits the WAVE complex to the plasma membrane to enable actin remodeling necessary for axon growth.
机译：神经元迁移和轴突生长，神经元发育期间的关键事件需要细胞骨架的不同变化。虽然已经鉴定并表征了许多极性的分子调节剂，但在这一过程中，对其生理作用是相对较少的。为了研究Rac1在神经元发展中的生理功能，我们已经产生了一种条件敲除小鼠，其中RAC1在整个大脑中被烧蚀。 RAC1缺乏的小脑颗粒神经元，其不表达其他RAC同种型，在体内和体外均显示神经元迁移和轴突形成受损。此外，RAC1消融破坏了生长锥中的层状斑层。 Rac1效应器的分析显示，从敲除生长锥体的质膜中没有Wiskott-Aldrich综合蛋白（WASP）族蛋白质蛋白质（波）复合物。波浪功能的丧失抑制了轴突生长，而膜系重波突变体的过度表达部分地拯救了RAC1敲除神经元的轴突生长。此外，波复合物效应器ARP2 / 3的药理抑制还降低了轴突生长。我们提出RAC1募集到质膜的波复合物，以使轴突生长所需的肌动蛋白改造。

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