ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Compensation of inositol 1,4,5-trisphosphate receptor function by altering sarco-endoplasmic reticulum calcium ATPase activity in the Drosophila flight circuit.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
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- Gαq splice variants mediate phototransduction, rhodopsin synthesis, and retinal integrity inThe Journal of biological chemistry · 2020Article
- Microtubules Stabilization by Mutant Spastin Affects ER Morphology and CaFrontiers in physiology · 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
- Neuronal Calcium Signaling in Metabolic Regulation and Adaptation to Nutrient Stress.Frontiers in neural circuits · 2018Review
- Control of protein translation by IPFly · 2017Article
- Store-independent modulation of Ca(2+) entry through Orai by Septin 7.Nature communications · 2016Article
- 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
- Patterning of wound-induced intercellular Ca(2+) flashes in a developing epithelium.Physical biology · 2015Article
- A single-cross, RNA interference-based genetic tool for examining the long-term maintenance of homeostatic plasticity.Frontiers in cellular neuroscience · 2015Article
- A genetic RNAi screen for IP₃/Ca²⁺ coupled GPCRs in Drosophila identifies the PdfR as a regulator of insect flight.PLoS genetics · 2013Article
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- Dynamin- and Rab5-dependent endocytosis is required to prevent Drosophila photoreceptor degeneration.Journal of cell science · 2011Article
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- The fragile X mental retardation protein developmentally regulates the strength and fidelity of calcium signaling in Drosophila mushroom body neurons.Neurobiology of disease · 2011Article
- Role of G-proteins in odor-sensing and CO2-sensing neurons in Drosophila.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Inositol 1,4,5-trisphosphate receptor and dSTIM function in Drosophila insulin-producing neurons regulates systemic intracellular calcium homeostasis and flight.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- The enigma of store-operated ca-entry in neurons: answers from the Drosophila flight circuit.Frontiers in neural circuits · 2010Article
- Intracellular Ca2+ signaling and store-operated Ca2+ entry are required in Drosophila neurons for flight.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Reduced odor responses from antennal neurons of G(q)alpha, phospholipase Cbeta, and rdgA mutants in Drosophila support a role for a phospholipid intermediate in insect olfactory transduction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ionic Ca2+ functions as a second messenger to control several intracellular processes. It also influences intercellular communication. The release of Ca2+ from intracellular stores through the inositol 1,4,5-trisphosphate receptor (InsP3R) occurs in both excitable and nonexcitable cells. In Drosophila, InsP3R activity is required in aminergic interneurons during pupal development for normal flight behavior. By altering intracellular Ca2+ and InsP3 levels through genetic means, we now show that signaling through the InsP3R is required at multiple steps for generating the neural circuit required in air puff-stimulated Drosophila flight. Decreased Ca2+ release in aminergic neurons during development of the flight circuit can be compensated by reducing Ca2+ uptake from the cytosol to intracellular stores. However, this mode of increasing intracellular Ca2+ is insufficient for maintenance of flight patterns over time periods necessary for normal flight. Our study suggests that processes such as maintenance of wing posture and formation of the flight circuit require InsP3 receptor function at a slow timescale and can thus be modulated by altering levels of cytosolic Ca2+ and InsP3. In contrast, maintenance of flight patterns probably requires fast modulation of Ca2+ levels, in which the intrinsic properties of the InsP3R play a pivotal role.
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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.