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R-Ras通过整合素连接激酶在糖原合酶激酶-3β上游控制轴突特化。

R-Ras controls axon specification upstream of glycogen synthase kinase-3beta through integrin-linked kinase.

作者信息

Oinuma Izumi, Katoh Hironori, Negishi Manabu

机构信息

Laboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.

出版信息

J Biol Chem. 2007 Jan 5;282(1):303-18. doi: 10.1074/jbc.M607979200. Epub 2006 Nov 15.

Abstract

The initial event in establishing a polarized neuron is the specification of a single axon. Spatially regulated glycogen synthase kinase-3beta (GSK-3beta) activity is critical for specifying axon-dendrite fate; however, the upstream signaling of GSK-3beta in the determination of neuronal polarity still remains obscure. Here, we found that, in cultured hippocampal neurons, the small GTPase R-Ras selectively localized in a single neurite of stage 2 neurons and that its activity increased after plating and peaked between stages 2 and 3. Ectopic expression of R-Ras induced global inactivation of GSK-3beta and formation of multiple axons, whereas knockdown of endogenous R-Ras by RNA interference blocked GSK-3beta inactivation and axon formation. GSK-3beta inactivation and axon formation by R-Ras required integrin-linked kinase (ILK), and subcellular localization of ILK was strictly regulated by R-Ras-mediated phosphatidylinositol 3-kinase activity. In addition, membrane targeting of ILK was sufficient to inactivate GSK-3beta and to form multiple axons. Our study demonstrates a novel role of R-Ras and ILK upstream of GSK-3beta in the regulation of neuronal polarity.

摘要

建立极化神经元的初始事件是单个轴突的特化。空间上受调控的糖原合酶激酶-3β(GSK-3β)活性对于确定轴突-树突命运至关重要;然而,GSK-3β在神经元极性确定中的上游信号传导仍不清楚。在这里,我们发现,在培养的海马神经元中,小GTP酶R-Ras选择性地定位于2期神经元的单个神经突中,并且其活性在铺板后增加,并在2期和3期之间达到峰值。R-Ras的异位表达诱导GSK-3β的整体失活和多个轴突的形成,而通过RNA干扰敲低内源性R-Ras则阻断了GSK-3β的失活和轴突形成。R-Ras导致的GSK-3β失活和轴突形成需要整合素连接激酶(ILK),并且ILK的亚细胞定位受到R-Ras介导的磷脂酰肌醇3激酶活性的严格调控。此外,ILK的膜靶向足以使GSK-3β失活并形成多个轴突。我们的研究证明了R-Ras和ILK在GSK-3β上游在神经元极性调控中的新作用。

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