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Synaptotagmin I functions as a calcium regulator of release probability.

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.

Pubmed ID: 11242035

Authors

  • Fernández-Chacón R
  • Königstorfer A
  • Gerber SH
  • García J
  • Matos MF
  • Stevens CF
  • Brose N
  • Rizo J
  • Rosenmund C
  • Südhof TC

Journal

Nature

Publication Data

March 1, 2001

Associated Grants

None

Mesh Terms

  • Animals
  • Calcium
  • Calcium-Binding Proteins
  • Cells, Cultured
  • Membrane Glycoproteins
  • Mice
  • Mutagenesis, Site-Directed
  • Nerve Tissue Proteins
  • Neurons
  • Neurotransmitter Agents
  • Point Mutation
  • Protein Binding
  • Protein Conformation
  • Synapses
  • Synaptic Vesicles
  • Synaptotagmin I
  • Synaptotagmins