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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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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.[1]

References

  1. Synaptotagmin I functions as a calcium regulator of release probability. Fernández-Chacón, R., Königstorfer, A., Gerber, S.H., García, J., Matos, M.F., Stevens, C.F., Brose, N., Rizo, J., Rosenmund, C., Südhof, T.C. Nature (2001) [Pubmed]
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