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Synchronous neurotransmitter release is triggered by Ca 2+  binding to the synaptic vesicle protein Synaptotagmin 1, while asynchronous fusion and short-term facilitation is hypothesized to be mediated by plasma membrane-localized Synaptotagmin 7 (SYT7). We generated mutations in  Drosophila Syt7  to determine if it plays a conserved role as the Ca 2+  sensor for these processes. Electrophysiology and quantal imaging revealed evoked release was elevated 2-fold.  Syt7  mutants also had a larger pool of readily-releasable vesicles, faster recovery following stimulation, and intact facilitation.  Syt1/Syt7  double mutants displayed more release than  Syt1  mutants alone, indicating SYT7 does not mediate the residual asynchronous release remaining in the absence of SYT1. SYT7 localizes to an internal membrane tubular network within the peri-active zone, but does not enrich at active zones. These findings indicate the two Ca 2+  sensor model of SYT1 and SYT7 mediating all phases of neurotransmitter release and facilitation is not applicable at  Drosophila  synapses.

Drosophila Synaptotagmin 7 negatively regulates synaptic vesicle release and replenishment in a dosage-dependent manner