ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Loss of flight and associated neuronal rhythmicity in inositol 1,4,5-trisphosphate receptor mutants of Drosophila.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 75 citations in OpenAlex.
- Synergism of IP3R and Parkin mutants identifies mitochondrial stress as an early feature of Parkinson's disease.Disease models & mechanisms · 2026Article
- Single-cell type analysis of wing premotor circuits in the ventral nerve cord ofbioRxiv : the preprint server for biology · 2025Article
- Monoaminergic Systems in Flight-Induced Potentiation of Phonotactic Behavior in Female CricketsInsects · 2024Article
- Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023Review
- Lysine acetylation regulates the interaction between proteins and membranes.Nature communications · 2021Article
- A Comparative Perspective on Functionally-Related, Intracellular Calcium Channels: The Insect Ryanodine and Inositol 1,4,5-Trisphosphate Receptors.Biomolecules · 2021Review
- The actin polymerization factor Diaphanous and the actin severing protein Flightless I collaborate to regulate sarcomere size.Developmental biology · 2021Article
- Article
- Microtubules Stabilization by Mutant Spastin Affects ER Morphology and CaFrontiers in physiology · 2019Article
- FMRFa receptor stimulated Ca2+ signals alter the activity of flight modulating central dopaminergic neurons in Drosophila melanogaster.PLoS genetics · 2018Article
- A pupal transcriptomic screen identifies Ral as a target of store-operated calcium entry in Drosophila neurons.Scientific reports · 2017Article
- Neurological and Motor Disorders: Neuronal Store-Operated CaAdvances in experimental medicine and biology · 2017Review
- Spontaneous CaFrontiers in molecular neuroscience · 2017Article
- Mutant IP3 receptors attenuate store-operated Ca2+ entry by destabilizing STIM-Orai interactions in Drosophila neurons.Journal of cell science · 2016Article
- Store-independent modulation of Ca(2+) entry through Orai by Septin 7.Nature communications · 2016Article
- Article
- The wavy Mutation Maps to the Inositol 1,4,5-Trisphosphate 3-Kinase 2 (IP3K2) Gene of Drosophila and Interacts with IP3R to Affect Wing Development.G3 (Bethesda, Md.) · 2015Article
- Impaired climbing and flight behaviour in Drosophila melanogaster following carbon dioxide anaesthesia.Scientific reports · 2015Article
- Store-Operated Calcium Entry through Orai Is Required for Transcriptional Maturation of the Flight Circuit in Drosophila.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Coordinated flight in winged insects requires rhythmic activity of the underlying neural circuit. Here, we show that Drosophila mutants for the inositol 1,4,5-trisphosphate (InsP(3)) receptor gene (itpr) are flightless. Electrophysiological recordings from thoracic indirect flight muscles show increased spontaneous firing accompanied by a loss of rhythmic flight activity patterns normally generated in response to a gentle puff of air. In contrast, climbing speed, the jump response, and electrical properties of the giant fiber pathway are normal, indicating that general motor coordination and neuronal excitability are much less sensitive to itpr mutations. All mutant phenotypes are rescued by expression of an itpr(+) transgene in serotonin and dopamine neurons. Pharmacological and immunohistochemical experiments support the idea that the InsP(3) receptor functions to modulate flight specifically through serotonergic interneurons. InsP(3) receptor action appears to be important for normal development of the flight circuit and its central pattern generator.
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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.