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Synaptotagmin I is necessary for compensatory synaptic vesicle endocytosis in vivo

Author

Listed:
  • Kira E. Poskanzer

    (University of California, San Francisco)

  • Kurt W. Marek

    (University of California, San Francisco)

  • Sean T. Sweeney

    (University of California, San Francisco)

  • Graeme W. Davis

    (University of California, San Francisco)

Abstract

Neurotransmission requires a balance of synaptic vesicle exocytosis and endocytosis1. Synaptotagmin I (Syt I) is widely regarded as the primary calcium sensor for synaptic vesicle exocytosis2,3,4,5,6. Previous biochemical data suggest that Syt I may also function during synaptic vesicle endocytosis7,8,9,10,11,12,13,14,15,16; however, ultrastructural analyses at synapses with impaired Syt I function have provided an indirect and conflicting view of the role of Syt I during synaptic vesicle endocytosis3,8,9,10,14. Until now it has not been possible experimentally to separate the exocytic and endocytic functions of Syt I in vivo. Here, we test directly the role of Syt I during endocytosis in vivo. We use quantitative live imaging of a pH-sensitive green fluorescent protein fused to a synaptic vesicle protein (synapto-pHluorin) to measure the kinetics of endocytosis in sytI-null Drosophila. We then combine live imaging of the synapto-pHluorins with photoinactivation of Syt I, through fluorescein-assisted light inactivation, after normal Syt I-mediated vesicle exocytosis. By inactivating Syt I only during endocytosis, we demonstrate that Syt I is necessary for the endocytosis of synaptic vesicles that have undergone exocytosis using a functional Syt I protein.

Suggested Citation

  • Kira E. Poskanzer & Kurt W. Marek & Sean T. Sweeney & Graeme W. Davis, 2003. "Synaptotagmin I is necessary for compensatory synaptic vesicle endocytosis in vivo," Nature, Nature, vol. 426(6966), pages 559-563, December.
    • Handle: RePEc:nat:nature:v:426:y:2003:i:6966:d:10.1038_nature02184
    DOI: 10.1038/nature02184
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