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External Ca²⁺ Dependency of Synaptic Transmission in Drosophila synaptotagmin I Mutants

Gunma University Graduate School of Medicine, Maebashi, Japan

Submitted 25 February 2005; accepted in final form 6 April 2005

To resolve some of differences in reports on the function of Synaptotagmin I (Syt I), we re-examined synaptic transmission at the neuromuscular junction of Drosophila embryos that have mutations in the Syt I gene (syt I). Two major questions addressed were which Ca²⁺ binding domain, C2A or C2B, sense Ca²⁺ and is Syt I a negative regulator of spontaneous vesicle fusion. Synaptic currents were induced by nerve stimulation or by high K⁺ treatment in external solutions containing various Ca²⁺ concentrations. In a null allele, syt I^AD4, synchronous synaptic currents were rarely observed but not abolished. The quantal content was about 1/60 of control but increased linearly with [Ca²⁺]_e with a slope of 0.95 (N) in the double logarithmic plot, in contrast to 3.01 in control. The slope of 1.06 in an allele, syt I^AD1, which lacks the second Ca²⁺ binding domain, C2B, was not different from in syt I^AD4. In another allele, syt I^AD3, in which one amino acid in C2B is mutated, synchronous synaptic transmission was also impaired and N was 1.54, which is significantly smaller than in control. In high K⁺ saline, the [Ca²⁺]_e dependency of vesicle release in syt I^AD4 was lower than in controls, whereas that in syt I^AD3 was even lower than in syt I^AD4, suggesting that syt I^AD3 is inhibiting vesicle fusion. These findings led us to conclude that C2B, not C2A, senses Ca²⁺, and Syt I is a negative regulator of vesicle fusion.

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