Jorgensen E M, Hartwieg E, Schuske K, Nonet M L, Jin Y, Horvitz H R
Department of Biology, University of Utah, Salt Lake City 84112, USA.
Nature. 1995 Nov 9;378(6553):196-9. doi: 10.1038/378196a0.
Synaptotagmin, an integral membrane protein of the synaptic vesicle, binds calcium and interacts with proteins of the plasma membrane. These observations suggest several possible functions for synaptotagmin in synaptic vesicle dynamics: it could facilitate exocytosis by promoting calcium-dependent fusion, inhibit exocytosis by preventing fusion, or facilitate endocytosis of synaptic vesicles from the plasma membrane by acting as a receptor for the endocytotic proteins of the clathrin AP2 complex. 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 or synaptic vesicles from the plasma membrane. Thus we propose that, as well as being involved in exocytosis, synaptotagmin functions in vesicular recycling.
突触结合蛋白是突触小泡的一种整合膜蛋白，可结合钙离子并与质膜蛋白相互作用。这些观察结果提示了突触结合蛋白在突触小泡动态变化中的几种可能功能：它可能通过促进钙依赖性融合来促进胞吐作用，通过阻止融合来抑制胞吐作用，或者通过作为网格蛋白AP2复合体的内吞蛋白的受体来促进突触小泡从质膜的内吞作用。在此我们表明，在秀丽隐杆线虫的突触结合蛋白突变体中，突触小泡在突触末端会耗尽。这种耗尽不是由运输缺陷或突触小泡释放增加引起的，而是由从质膜回收突触小泡的缺陷导致的。因此我们提出，除了参与胞吐作用外，突触结合蛋白还在小泡循环中发挥作用。
