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Synaptotagmin I Functions as a Calcium Sensor to Synchronize Neurotransmitter Release
To characterize Ca 2+-mediated synaptic vesicle fusion, we analyzed Drosophila synaptotagmin I mutants deficient in specific interactions mediated by its two Ca 2+ binding C2 domains. In the absence of synaptotagmin I, synchronous release is abolished and a kinetically distinct delayed asynchronous...
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Published in: | Neuron (Cambridge, Mass.) Mass.), 2002-12, Vol.36 (5), p.897-908 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | To characterize Ca
2+-mediated synaptic vesicle fusion, we analyzed
Drosophila synaptotagmin I mutants deficient in specific interactions mediated by its two Ca
2+ 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 Ca
2+ cooperativity. Mutants that disrupt Ca
2+ sensing by the C2B domain have synchronous release with normal Ca
2+ cooperativity, but with reduced release probability. Our data suggest the Ca
2+ 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 Ca
2+ sensor for evoked release and functions to trigger synchronous fusion in response to Ca
2+, while suppressing asynchronous release. |
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ISSN: | 0896-6273 1097-4199 |
DOI: | 10.1016/S0896-6273(02)01065-6 |