A Temperature-Sensitive Paralytic Mutant Defines a Primary Synaptic Calcium Channel inDrosophila

Neurotransmission at chemical synapses involves regulated exocytosis of neurotransmitter from the presynaptic terminal. Neurotransmitter release is thought to be triggered by calcium influx through specific classes of voltage-gated calcium channels. Here we report genetic and functional analysis implicating a specific calcium channel gene product in neurotransmitter release. We have isolated a temperature-sensitive paralytic allele of the Drosophila calcium channel α1 subunit gene, cacophony ( cac ). This mutant, referred to as cac TS2 , allows functional analysis of synaptic transmission after acute perturbation of a specific α1 subunit. Electrophysiological analysis at neuromuscular synapses revealed that neurotransmitter release in cac TS2 is markedly reduced at elevated temperatures, indicating that cac encodes a primary α1 subunit functioning in synaptic transmission. These observations further define the molecular basis of voltage-gated calcium entry at synapses and provide a new starting point for further genetic analysis of synaptic mechanisms.