ArticlePloS one2009
Inositol 1,4,5- trisphosphate receptor function in Drosophila insulin producing cells.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- The role of septin 7 in physiology and pathological disease: A systematic review of current status.Journal of cellular and molecular medicine · 2018Pooled it
- Transcriptome Analysis of the Brain and Gnathal Ganglion Reveals Feeding-Mediated Genes inBiomolecules · 2026Article
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- ER-Ca2+ sensor STIM regulates neuropeptides required for development under nutrient restriction in Drosophila.PloS one · 2019Article
- IPDevelopment (Cambridge, England) · 2017Article
- Article
- 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
- 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
- Molecular heterochrony and the evolution of sociality in bumblebees (Bombus terrestris).Proceedings. Biological sciences · 2014Article
- Loss of IP3 receptor function in neuropeptide secreting neurons leads to obesity in adult Drosophila.BMC neuroscience · 2013Article
- Altered lipid homeostasis in Drosophila InsP3 receptor mutants leads to obesity and hyperphagia.Disease models & mechanisms · 2013Article
- Activation of PLC by an endogenous cytokine (GBP) in Drosophila S3 cells and its application as a model for studying inositol phosphate signalling through ITPK1.The Biochemical journal · 2012Article
- Insulin-producing cells in the brain of adult Drosophila are regulated by the serotonin 5-HT1A receptor.Cellular and molecular life sciences : CMLS · 2012Article
- Identification of a novel hemolymph peptide that modulates silkworm feeding motivation.The Journal of biological chemistry · 2011Article
- Article
- 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
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The Inositol 1,4,5- trisphosphate receptor (InsP(3)R) is an intracellular ligand gated channel that releases calcium from intracellular stores in response to extracellular signals. To identify and understand physiological processes and behavior that depends on the InsP(3) signaling pathway at a systemic level, we are studying Drosophila mutants for the InsP(3)R (itpr) gene. Here, we show that growth defects precede larval lethality and both are a consequence of the inability to feed normally. Moreover, restoring InsP(3)R function in insulin producing cells (IPCs) in the larval brain rescues the feeding deficit, growth and lethality in the itpr mutants to a significant extent. We have previously demonstrated a critical requirement for InsP(3)R activity in neuronal cells, specifically in aminergic interneurons, for larval viability. Processes from the IPCs and aminergic domain are closely apposed in the third instar larval brain with no visible cellular overlap. Ubiquitous depletion of itpr by dsRNA results in feeding deficits leading to larval lethality similar to the itpr mutant phenotype. However, when itpr is depleted specifically in IPCs or aminergic neurons, the larvae are viable. These data support a model where InsP(3)R activity in non-overlapping neuronal domains independently rescues larval itpr phenotypes by non-cell autonomous mechanisms.
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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.