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• W2083888682 abstract "Synaptotagmin I, a calcium-binding synaptic vesicle protein, is thought to act as the calcium sensor for fast neurotransmission, but what synaptotagmin I does, upon binding calcium, to trigger exocytosis is still unknown. To begin to examine the role of synaptotagmin I's interactions with calcium-dependent binding partners, three mutant versions of synaptotagmin I reported to affect calcium-dependent self-oligomerization (Y311N, K327A, and K326/327A) were expressed in cultured mouse hippocampal neurons lacking endogenous synaptotagmin I, and effects on neurotransmission were evaluated by comparison with transmission rescued by wild-type synaptotagmin I. All three mutants reduced transmitter release. To separate effects on calcium binding from effects on calcium-dependent oligomerization, we measured the calcium dependence of exocytosis for two of the mutants. Both showed apparent calcium affinity much lower than wild-type, a reduction sufficient to account for the neurotransmission defects. We conclude that self-oligomerization is unlikely to play any significant role in triggering synaptic vesicle exocytosis." @default.
• W2083888682 created "2016-06-24" @default.
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• W2083888682 date "2005-07-01" @default.
• W2083888682 modified "2023-10-18" @default.
• W2083888682 title "Synaptotagmin mutants Y311N and K326/327A alter the calcium dependence of neurotransmission" @default.
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• W2083888682 doi "https://doi.org/10.1016/j.mcn.2005.03.015" @default.
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