Defective recycling of synaptic vesicles in synaptotagmin mutants of caenorhabditis elegans

Erik M. Jorgensen, Erika Hartwieg, Kim Schuske, Michael L. Nonet, Yishi Jin, H. Robert Horvitz

Research output: Contribution to journalArticlepeer-review

260 Scopus citations

Abstract

SYNAPTOTAGMIN, an integral membrane protein of the synaptic vesicle1,2, binds calcium and interacts with proteins of the plasma membrane4–6. These observations suggest several possible functions for synaptotagmin in synaptic vesicle dynamics: it could facilitate exocytosis by promoting calcium-dependent fusion3, inhibit exocytosis by preventing fusion7, or facilitate endocytosis of synaptic vesicles from the plasma membrane by acting as a receptor for the endocytotic proteins of the clathrin AP2 complex8. 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.

Original languageEnglish
Pages (from-to)196-199
Number of pages4
JournalNature
Volume378
Issue number6553
DOIs
StatePublished - Nov 9 1995

Fingerprint

Dive into the research topics of 'Defective recycling of synaptic vesicles in synaptotagmin mutants of caenorhabditis elegans'. Together they form a unique fingerprint.

Cite this