Synaptotagmin I functions as a calcium regulator of release probability
2001 | journal article; research paper. A publication with affiliation to the University of Göttingen.
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- Authors
- Fernandez-Chacon, R; Königstorfer, A.; Gerber, S. H.; Garcia, J; Matos, M. F.; Stevens, C. F.; Brose, Nils ; Rizo, Josep; Rosenmund, C.; Suedhof, Thomas C.
- 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.
- Issue Date
- 2001
- Publisher
- Macmillan Publishers Ltd
- Journal
- Nature
- ISSN
- 0028-0836