Synaptotagmin I functions as a calcium regulator of release probability

Rafael Fernández-Chacón, Andreas Königstorfer, Stefan H. Gerber, Jesús García, Maria F. Matos, Charles F. Stevens, Nils Brose, Josep Rizo, Christian Rosenmund and Thomas C. Südhof ()
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Rafael Fernández-Chacón: Center for Basic Neuroscience, and Howard Hughes Medical Institute, The University of Texas Southwestern Medical Center
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

Nature, 2001, vol. 410, issue 6824, 41-49

Abstract: 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.

Date: 2001
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DOI: 10.1038/35065004

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