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

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)4885-4889
Number of pages5
JournalJournal of Neuroscience
Volume20
Issue number13
StatePublished - Jul 1 2000

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Calcium Channels
Drosophila
Neurotransmitter Agents
Synaptic Transmission
Synapses
Temperature
Calcium
Exocytosis
Presynaptic Terminals
Genes
Alleles

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

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title = "A temperature-sensitive paralytic mutant defines a primary synaptic calcium channel in Drosophila",
abstract = "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.",
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A temperature-sensitive paralytic mutant defines a primary synaptic calcium channel in Drosophila. / Kawasaki, Fumiko; Felling, Ryan; Ordway, Richard W.

In: Journal of Neuroscience, Vol. 20, No. 13, 01.07.2000, p. 4885-4889.

Research output: Contribution to journalArticle

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AB - 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.

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