Defects in synaptic vesicle docking in unc-18 mutants
Defects in synaptic vesicle docking in unc-18 mutants
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DOI：
10.1038/nn1118
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发表时间：
2003-10-01
影响因子：
25
通讯作者：
Jorgensen, EM
中科院分区：
文献类型：
--
作者：
Weimer, RM;Richmond, JE;Jorgensen, EM
Sec1 相关蛋白在真核细胞的大多数（如果不是全部）膜运输途径中发挥作用。神经元突触小泡胞吐作用所需的 Sec1 相关蛋白是 UNC-18。囊泡胞吐作用期间 UNC-18 功能的几种模型正在考虑中。我们通过表征线虫秀丽隐杆线虫的 unc-18 突变体来测试这些模型。在没有 UNC-18 的情况下，易于释放的池的大小会严重减小。我们的结果表明，具有融合能力的囊泡几乎不存在并不是由于突触蛋白水平降低、突触蛋白定位错误、融合缺陷或引发期间未能打开突触蛋白引起的。相反，我们发现 unc-18 突变体活性区的对接囊泡减少，这表明 UNC-18 直接或间接地充当囊泡对接的促进剂。
Sec1-related proteins function in most, if not all, membrane trafficking pathways in eukaryotic cells. The Sec1-related protein required in neurons for synaptic vesicle exocytosis is UNC-18. Several models for UNC-18 function during vesicle exocytosis are under consideration. We have tested these models by characterizing unc-18 mutants of the nematode Caenorhabditis elegans. In the absence of UNC-18, the size of the readily releasable pool is severely reduced. Our results show that the near absence of fusion-competent vesicles is not caused by a reduction in syntaxin levels, by a mislocalization of syntaxin, by a defect in fusion or by a failure to open syntaxin during priming. Rather, we found a reduction of docked vesicles at the active zone in unc-18 mutants, suggesting that UNC-18 functions, directly or indirectly, as a facilitator of vesicle docking.