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Defective recycling of synaptic vesicles in synaptotagmin mutants of Caenorhabditis elegans

Nature volume 378, pages 196199 (09 November 1995) | Download Citation

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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.

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Author information

Affiliations

  1. Department of Biology, University of Utah, Salt Lake City, Utah 84112, USA

    • Erik M. Jorgensen
    •  & Kim Schuske
  2. Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA

    • Erik M. Jorgensen
    • , Erika Hartwieg
    • , Yishi Jin
    •  & H. Robert Horvitz
  3. Department of Anatomy and Neurobiology, Washington University School of Medicine, St Louis, Missouri 63110, USA

    • Michael L. Nonet

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https://doi.org/10.1038/378196a0

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