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The Journal of Neuroscience, July 1, 2000, 20(13):4885-4889

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

Fumiko Kawasaki, Ryan Felling, and Richard W. Ordway

Department of Biology, The Pennsylvania State University, University Park, Pennsylvania 16802

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 alpha 1 subunit gene, cacophony (cac). This mutant, referred to as cacTS2, allows functional analysis of synaptic transmission after acute perturbation of a specific alpha 1 subunit. Electrophysiological analysis at neuromuscular synapses revealed that neurotransmitter release in cacTS2 is markedly reduced at elevated temperatures, indicating that cac encodes a primary alpha 1 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.

Key words: calcium channel; neurotransmitter release; synaptic transmission; cacophony; Drosophila; temperature-sensitive

Copyright © 2000 Society for Neuroscience  0270-6474/00/20134885-05$05.00/0


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