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Synaptotagmin I functions as a calcium regulator of release probability

Author

Listed:
  • Rafael Fernández-Chacón

    (Center for Basic Neuroscience, and Howard Hughes Medical Institute, The University of Texas Southwestern Medical Center
    Max-Planck-Institut für biophysikalische Chemie)

  • Andreas Königstorfer

    (Max-Planck-Institut für experimentelle Medizin)

  • Stefan H. Gerber

    (Center for Basic Neuroscience, and Howard Hughes Medical Institute, The University of Texas Southwestern Medical Center)

  • Jesús García

    (The University of Texas Southwestern Medical Center)

  • Maria F. Matos

    (Center for Basic Neuroscience, and Howard Hughes Medical Institute, The University of Texas Southwestern Medical Center)

  • Charles F. Stevens

    (The Salk Institute, and Howard Hughes Medical Institute)

  • Nils Brose

    (Max-Planck-Institut für experimentelle Medizin)

  • Josep Rizo

    (The University of Texas Southwestern Medical Center)

  • Christian Rosenmund

    (Max-Planck-Institut für biophysikalische Chemie)

  • Thomas C. Südhof

    (Center for Basic Neuroscience, and Howard Hughes Medical Institute, The University of Texas Southwestern Medical Center)

Abstract

In all synapses, Ca2+ triggers neurotransmitter release to initiate signal transmission. Ca2+ presumably acts by activating synaptic Ca2+ sensors, but the nature of these sensors—which are the gatekeepers to neurotransmission—remains unclear. One of the candidate Ca2+ sensors in release is the synaptic Ca2+-binding protein synaptotagmin I. Here we have studied a point mutation in synaptotagmin I that causes a twofold decrease in overall Ca2+ affinity without inducing structural or conformational changes. When introduced by homologous recombination into the endogenous synaptotagmin I gene in mice, this point mutation decreases the Ca2+ sensitivity of neurotransmitter release twofold, but does not alter spontaneous release or the size of the readily releasable pool of neurotransmitters. Therefore, Ca2+ binding to synaptotagmin I participates in triggering neurotransmitter release at the synapse.

Suggested Citation

  • Rafael Fernández-Chacón & Andreas Königstorfer & Stefan H. Gerber & Jesús García & Maria F. Matos & Charles F. Stevens & Nils Brose & Josep Rizo & Christian Rosenmund & Thomas C. Südhof, 2001. "Synaptotagmin I functions as a calcium regulator of release probability," Nature, Nature, vol. 410(6824), pages 41-49, March.
    • Handle: RePEc:nat:nature:v:410:y:2001:i:6824:d:10.1038_35065004
    DOI: 10.1038/35065004
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