神经胶质细胞成熟因子β(GMFB)在物种间高度保守，但功能不清，前期研究发现，敲除GMFB后，斑马鱼运动功能减弱，其放射状胶质细胞（神经干细胞）纤维丝变粗、短、排列无序、缺乏方向性，机械损伤后，斑马鱼神经再生能力降低，其机理为GMFB的敲除抑制了放射状神经胶质细胞I 型向II型的转化。进一步采用免疫共沉淀和质谱分析发现，GMFB与接触蛋白-1(CNTN-1)，actin，tubulin一起共沉淀，因此我们推测GMFB通过与CNTN-1结合调控细胞骨架，特别是神经微管的形成，进而影响了神经的再生。本课题将通过酵母双杂交系统，提供GMFB与CNTN-1结合的直接证据，通过pull down技术寻找GMFB蛋白与CNTN-1蛋白的结合区域，并合成结合区域的干扰肽，抑制这种结合，以证实我们的推测，这些结果将明确GMFB的功能，为斑马鱼神经再生功能的研究，也为哺乳动物缺乏神经再生能力的研究提供思路。

The glial cell maturation factor β (GMB) is highly conserved among species, but the function is unclear. Our previous study found that the GMFB knockdown in zebrafish would reduceits motor function, and the radial glial cells (neural stem cells) become thick, short, disorder and lack of direction.The ability of nerve regeneration in GMFB knockdown zebrafishdecreased post mechanical damage, GMFB knockout inhibited thetransformation of radial glial cells from type I to type II. The immunoprecipitation and mass spectrometry analysis showed that GMFB co-precipitated with contact protein-1 (CNTN-1), actin and tubulin, so we speculated that GMFB might regulate the cytoskeleton, especially the formation of neural microtubules through CNTN-1and then affectedthe nerveregeneration. In this study, the direct evidence of GMFB binding to CNTN-1 will be provided by the yeast two-hybrid system, and the proteinbinding region of GMFB and CNTN-1 will be found by pull down technique. Our hypothesiswill be confirmed by inhibitingthe combinationof GMFB and CNTN-1 with designed Interferepeptide. These results will clarify theGMFB function, and provide the potential mechanism analysis for nerve regeneration in zebrafish and the lack of nerve regeneration in mammals .