期刊
JOURNAL OF CELL BIOLOGY
卷 205, 期 1, 页码 21-31出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201312109
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资金
- National Institutes of Health [RO1EY018884, 5R01-GM088803]
- Welch Foundation [I-1657, Q-581]
Most chemical neurotransmission occurs through Ca2+-dependent evoked or spontaneous vesicle exocytosis. In both cases, Ca2+ sensing is thought to occur shortly before exocytosis. In this paper, we provide evidence that the Ca2+ dependence of spontaneous vesicle release may partly result from an earlier requirement of Ca2+ for the assembly of soluble Nethylmaleimide sensitive fusion attachment protein receptor (SNARE) complexes. We show that the neuronal vacuolar-type H+-adenosine triphosphatase V0 subunit al (V100) can regulate the formation of SNARE complexes in a Ca2+-Calmodulin (CaM)-dependent manner. Ca2+-CaM regulation of V100 is not required for vesicle acidification. Specific disruption of the Ca2+-dependent regulation of V100 by CaM led to a >90% loss of spontaneous release but only had a mild effect on evoked release at Drosophila melanogaster embryo neuromuscular junctions. Our data suggest that Ca2+ CaM regulation of V100 may control SNARE complex assembly for a subset of synaptic vesicles that sustain spontaneous release.
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