DEFECTIVE RECYCLING OF SYNAPTIC VESICLES IN SYNAPTOTAGMIN MUTANTS OF CAENORHABDITIS-ELEGANS
DEFECTIVE RECYCLING OF SYNAPTIC VESICLES IN SYNAPTOTAGMIN MUTANTS OF CAENORHABDITIS-ELEGANS
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DOI：
10.1038/378196a0
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发表时间：
1995-11-09
期刊：
影响因子：
64.8
通讯作者：
HORVITZ, HR
中科院分区：
文献类型：
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作者：
JORGENSEN, EM;HARTWIEG, E;HORVITZ, HR
突触囊泡（1，2）的一种整合膜蛋白，突触膜蛋白结合钙并与质膜蛋白相互作用（4-6）。这些观察结果表明突触结合蛋白在突触囊泡动力学中的几种可能功能：它可以通过促进钙依赖性融合来促进胞吐作用（3），通过阻止融合来抑制胞吐作用（7），或通过充当网格蛋白AP 2复合物的内吞蛋白的受体来促进突触囊泡从质膜的内吞作用（8）。在这里，我们表明，突触囊泡耗尽在突触末端的突触结合蛋白突变体的线虫秀丽隐杆线虫。这种消耗不是由运输缺陷或突触囊泡释放增加引起的，而是由突触囊泡从质膜中回收的缺陷引起的。因此，我们建议，以及参与胞吐，突触结合蛋白功能囊泡回收。
SYNAPTOTAGMIN, an integral membrane protein of the synaptic vesicle(1,2), binds calcium and interacts with proteins of the plasma membrane(4-6). These observations suggest several possible functions for synaptotagmin in synaptic vesicle dynamics: it could facilitate exocytosis by promoting calcium-dependent fusion(3), inhibit exocytosis by preventing fusion(7), or facilitate endocytosis of synaptic vesicles from the plasma membrane by acting as a receptor for the endocytotic proteins of the clathrin AP2 complex(8). Here we show that synaptic vesicles are depleted at synaptic terminals in synaptotagmin mutants of the nematode Caenorhabditis elegans. This depletion is not caused by a defect in transport or by increased synaptic vesicle release, but rather by a defect in retrieval of synaptic vesicles from the plasma membrane. Thus we propose that, as well as being involved in exocytosis, synaptotagmin functions in vesicular recycling.