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Collapsin response mediator protein-2 regulates neurite formation by modulating tubulin GTPase activity

机译：胶原蛋白介导蛋白2通过调节微管蛋白GTPase活性来调节神经突的形成

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摘要

Collapsin response mediator protein-2 (CRMP-2) plays a key role in axonal development by regulating microtubule dynamics. However, the molecular mechanisms underlying this function have not been clearly elucidated. In this study, we demonstrated that hCRMP-2, specifically amino acid residues 480-509, is essential for stimulating tubulin GTPase activity. We also found that the GTPase-activating protein (GAP) activity of hCRMP-2 was important for microtubule assembly and neurite formation in differentiated PC12 pheochromocytoma cell lines. Mutant hCRMP-2, lacking arginine residues responsible for GAP activity, inhibited microtubule assembly and neurite formation. Interestingly, we found that the N-terminal region (amino acids 150-299) of hCRMP-2 had an inhibitory role on GAP activity via a direct interaction with the C-terminal region (amino acids 480-509). Our results suggest that CRMP-2 as a tubulin direct binder may be a GAP of tubulin in neurite formation and that its CAP activity may be regulated by an intramolecular interaction with an N-terminal inhibitory region.
机译：Collapsin反应介质蛋白2（CRMP-2）通过调节微管动力学在轴突发育中起关键作用。但是，尚未清楚阐明该功能的分子机制。在这项研究中，我们证明了hCRMP-2，特别是氨基酸残基480-509，对于刺激微管蛋白GTPase活性至关重要。我们还发现hCRMP-2的GTP酶激活蛋白（GAP）活性对于分化的PC12嗜铬细胞瘤细胞系中的微管组装和神经突形成很重要。突变的hCRMP-2，缺少负责GAP活性的精氨酸残基，抑制了微管的组装和神经突的形成。有趣的是，我们发现hCRMP-2的N末端区域（氨基酸150-299）通过与C末端区域（氨基酸480-509）的直接相互作用对GAP活性具有抑制作用。我们的结果表明CRMP-2作为微管蛋白直接结合剂可能是微管蛋白在神经突形成中的GAP，其CAP活性可能受与N端抑制区的分子内相互作用的调节。

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