A temperature-sensitive paralytic mutant defines a primary synaptic calcium channel in Drosophila

Neurotransmission at chemical synapses involves regulated exocytosis of neu rotransmitter from the presynaptic terminal. Neurotransmitter release is th ought to be triggered by calcium influx through specific classes of voltage -gated calcium channels. Here we report genetic and functional analysis imp licating a specific calcium channel gene product in neurotransmitter releas e. We have isolated a temperature-sensitive paralytic allele of the Drosoph ila calcium channel alpha 1 subunit gene, cacophony (cac). This mutant, ref erred to as cac(TS2), allows functional analysis of synaptic transmission a fter acute perturbation of a specific alpha 1 subunit. Electrophysiological analysis at neuromuscular synapses revealed that neurotransmitter release in cas(TS2) is markedly reduced at elevated temperatures, indicating that c ac encodes a primary alpha 1 subunit functioning in synaptic transmission. These observations further define the molecular basis of voltage-gated calc ium entry at synapses and provide a new starting point for further genetic analysis of synaptic mechanisms.