NEURONAL PATHFINDING IS ABNORMAL IN MICE LACKING THE NEURONAL GROWTH CONE PROTEIN GAP-43
NEURONAL PATHFINDING IS ABNORMAL IN MICE LACKING THE NEURONAL GROWTH CONE PROTEIN GAP-43
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DOI：
10.1016/0092-8674(95)90495-6
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发表时间：
1995-02-10
期刊：
影响因子：
64.5
通讯作者：
FISHMAN, MC
中科院分区：
文献类型：
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作者：
STRITTMATTER, SM;FANKHAUSER, C;FISHMAN, MC
GAP-43被称为“生长”或“可塑性”蛋白，因为它在发育和轴突再生期间在神经元生长锥中以高水平表达。通过同源重组，我们产生了缺乏GAP-43的小鼠。小鼠在出生后早期死亡。缺乏GAP-43的视网膜轴突仍然被困在交叉中6天，无法导航通过这个中线决定点。在随后的几周里，大多数缺乏GAP-43的轴突确实进入了适当的神经束，成年人的中枢神经系统基本正常。没有证据表明干扰神经生长速率，培养的神经元以与对照组难以区分的方式延伸神经突和生长锥。因此，差距-43蛋白对于轴突生长或生长锥形成本身不是必需的，但在某些决定点（例如视交叉）是必需的。这与GAP-43用于放大来自生长锥的寻路信号的假设是一致的。
GAP-43 has been termed a ''growth'' or ''plasticity'' protein because it is expressed at high levels in neuronal growth cones during development and during axonal regeneration. By homologous recombination, we generated mice lacking GAP-43. The mice die in the early postnatal period. GAP-43-deficient retinal axons remain trapped in the chiasm for 6 days, unable to navigate past this midline decision point. Over the subsequent weeks of life, most GAP-43-deficient axons do enter the appropriate tracts, and the adult CNS is grossly normal. There is no evidence for interference with nerve growth rate, and cultured neurons extend neurites and growth cones in a fashion indistinguishable from controls. Thus, the GAP-43 protein is not essential for axonal outgrowth or growth cone formation pet se, but is required at certain decision points, such as the optic chiasm. This is compatible with the hypothesis that GAP-43 serves to amplify pathfinding signals from the growth cone.