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- W1963551844 abstract "To characterize Ca2+-mediated synaptic vesicle fusion, we analyzed Drosophila synaptotagmin I mutants deficient in specific interactions mediated by its two Ca2+ binding C2 domains. In the absence of synaptotagmin I, synchronous release is abolished and a kinetically distinct delayed asynchronous release pathway is uncovered. Synapses containing only the C2A domain of synaptotagmin partially recover synchronous fusion, but have an abolished Ca2+ cooperativity. Mutants that disrupt Ca2+ sensing by the C2B domain have synchronous release with normal Ca2+ cooperativity, but with reduced release probability. Our data suggest the Ca2+ cooperativity of neurotransmitter release is likely mediated through synaptotagmin-SNARE interactions, while phospholipid binding and oligomerization trigger rapid fusion with increased release probability. These results indicate that synaptotagmin is the major Ca2+ sensor for evoked release and functions to trigger synchronous fusion in response to Ca2+, while suppressing asynchronous release." @default.
- W1963551844 created "2016-06-24" @default.
- W1963551844 creator A5080418424 @default.
- W1963551844 creator A5083466248 @default.
- W1963551844 date "2002-12-01" @default.
- W1963551844 modified "2023-10-06" @default.
- W1963551844 title "Synaptotagmin I Functions as a Calcium Sensor to Synchronize Neurotransmitter Release" @default.
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- W1963551844 doi "https://doi.org/10.1016/s0896-6273(02)01065-6" @default.
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