| First Author | Fernández-Chacón R | Year | 2001 |
| Journal | Nature | Volume | 410 |
| Issue | 6824 | Pages | 41-9 |
| PubMed ID | 11242035 | Mgi Jnum | J:76452 |
| Mgi Id | MGI:2179533 | Doi | 10.1038/35065004 |
| Citation | Fernandez-Chacon R, et al. (2001) Synaptotagmin I functions as a calcium regulator of release probability. Nature 410(6824):41-9 |
| abstractText | 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. |
