Synaptotagmin I functions as a calcium regulator of release probability
Synaptotagmin I functions as a calcium regulator of release probability
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DOI：
10.1038/35065004
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发表时间：
2001-03-01
期刊：
影响因子：
64.8
通讯作者：
Südhof, TC
中科院分区：
文献类型：
--
作者：
Fernández-Chacón, R;Königstorfer, A;Südhof, TC
在所有突触中，Ca 2+触发神经递质释放以启动信号传递。Ca 2+可能通过激活突触Ca 2+传感器起作用，但这些传感器的性质-神经传递的看门人-仍然不清楚。其中一个候选的钙释放传感器是突触钙结合蛋白synaptotagmin I。在这里，我们已经研究了一个点突变的synaptotagmin I，导致整体钙离子亲和力的两倍下降，而不诱导结构或构象的变化。当通过同源重组引入小鼠内源性突触结合蛋白I基因时，该点突变使神经递质释放的Ca 2+敏感性降低两倍，但不改变自发释放或容易释放的神经递质池的大小。因此，Ca 2+结合到突触结合蛋白I参与触发突触处的神经递质释放。
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.