ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Synaptic calcium-channel function in Drosophila: analysis and transformation rescue of temperature-sensitive paralytic and lethal mutations of cacophony.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 93 citations in OpenAlex.
- Building and modifying diverse synaptic properties: Insights from Drosophila.Current opinion in neurobiology · 2025Review
- Specific presynaptic functions require distincteLife · 2025Article
- Homeostatic synaptic plasticity rescues neural coding reliability.Nature communications · 2023Article
- Interactive nanocluster compaction of the ELKS scaffold and Cacophony CaScience advances · 2023Article
- Regulation of excitation-contraction coupling at the Drosophila neuromuscular junction.The Journal of physiology · 2022Article
- Genetic analysis of the Drosophila ESCRT-III complex protein, VPS24, reveals a novel function in lysosome homeostasis.PloS one · 2021Article
- Homeostatic Depression Shows Heightened Sensitivity to Synaptic Calcium.Frontiers in cellular neuroscience · 2021Article
- Endogenous Tagging Reveals Differential Regulation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Glutamate signaling at cytoneme synapses.Science (New York, N.Y.) · 2019Article
- Deletion of a specific exon in the voltage-gated calcium channel geneThe Journal of experimental biology · 2019Article
- Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway.PLoS genetics · 2018Article
- t-GRASP, a targeted GRASP for assessing neuronal connectivity.Journal of neuroscience methods · 2018Article
- The CaScientific reports · 2018Article
- Coupling the Structural and Functional Assembly of Synaptic Release Sites.Frontiers in neuroanatomy · 2018Review
- Dendritic and Axonal L-Type Calcium Channels Cooperate to Enhance Motoneuron Firing Output duringThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- FlpStop, a tool for conditional gene control ineLife · 2017Article
- Fife organizes synaptic vesicles and calcium channels for high-probability neurotransmitter release.The Journal of cell biology · 2017Article
- Exploring the Interaction ofJournal of experimental neuroscience · 2017Article
- Mutations of the Calcium Channel Gene cacophony Suppress Seizures in Drosophila.PLoS genetics · 2016Article
- A Distinct Perisynaptic Glial Cell Type Forms Tripartite Neuromuscular Synapses in the Drosophila Adult.PloS one · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated calcium channels play a key role in chemical synaptic transmission by providing the calcium trigger for regulated neurotransmitter release. Genes encoding the primary structural subunit, alpha1, as well as accessory subunits of presynaptic calcium channels have now been identified in a variety of organisms. The cacophony (cac) gene in Drosophila, also known as nightblind A, encodes a voltage-gated calcium-channel alpha1 subunit homologous to vertebrate alpha1 subunits implicated in neurotransmitter release. A recent genetic screen in our laboratory isolated cac(TS2), a conditional cac mutant exhibiting rapid paralysis at elevated temperatures. This mutant has allowed synaptic electrophysiology after acute perturbation of a specific calcium-channel gene product, demonstrating that cac encodes a primary calcium channel functioning in neurotransmitter release. Here we report the molecular lesion in cac(TS2), a missense mutation within a calcium-dependent regulatory domain of the alpha1 subunit, as well as phenotypic rescue of temperature-sensitive and lethal cac mutations by transgenic expression of a wild-type cac cDNA. Notably, rescue of rapid, calcium-triggered neurotransmitter release was achieved by neural expression of a single cDNA containing a subset of alternative exons and lacking any conserved synaptic-protein interaction sequence. Possible implications of these findings are discussed in the context of structure-function studies of synaptic calcium channels, as well as alternative splicing and mRNA editing of the cac transcript.
Indexed as
Identifiers
12122048PMC6757926W1913041806What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.