ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Drosophila fragile X mental retardation protein and metabotropic glutamate receptor A convergently regulate the synaptic ratio of ionotropic glutamate receptor subclasses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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39 citing papers in PubMed.
- Review
- Genetic analyses enabled by the fourth chromosome resource project reveal unexpected mutant phenotypes and suggest new disease models.G3 (Bethesda, Md.) · 2026Article
- Interaction between neuromuscular junction metabolic requirements in fragile X syndrome and glycogen storage disease models.Disease models & mechanisms · 2025Article
- FMR1 genetically interacts with DISC1 to regulate glutamatergic synaptogenesis.Schizophrenia (Heidelberg, Germany) · 2024Article
- Activation of the 5-HT1A Receptor by Eltoprazine Restores Mitochondrial and Motor Deficits in aInternational journal of molecular sciences · 2024Article
- RNA-binding FMRP and Staufen sequentially regulate the Coracle scaffold to control synaptic glutamate receptor and bouton development.Development (Cambridge, England) · 2022Article
- Dysregulation of BMP, Wnt, and Insulin Signaling in Fragile X Syndrome.Frontiers in cell and developmental biology · 2022Review
- Postsynaptic cAMP signalling regulates the antagonistic balance ofDevelopment (Cambridge, England) · 2020Article
- Wnd/DLK Is a Critical Target of FMRP Responsible for Neurodevelopmental and Behavior Defects in the Drosophila Model of Fragile X Syndrome.Cell reports · 2019Article
- Molecular Biomarkers in Fragile X Syndrome.Brain sciences · 2019Review
- Fragile X Mental Retardation Protein Regulates Activity-Dependent Membrane Trafficking andFrontiers in molecular neuroscience · 2017Review
- Multiple Drug Treatments That Increase cAMP Signaling Restore Long-Term Memory and Aberrant Signaling in Fragile X Syndrome Models.Frontiers in behavioral neuroscience · 2016Article
- Transmission, Development, and Plasticity of Synapses.Genetics · 2015Review
- Synergistic interactions between Drosophila orthologues of genes spanned by de novo human CNVs support multiple-hit models of autism.PLoS genetics · 2015Article
- Article
- Impaired activity-dependent neural circuit assembly and refinement in autism spectrum disorder genetic models.Frontiers in cellular neuroscience · 2014Review
- Fragile X mental retardation protein regulates trans-synaptic signaling in Drosophila.Disease models & mechanisms · 2013Article
- The cell polarity scaffold Lethal Giant Larvae regulates synapse morphology and function.Journal of cell science · 2013Article
- The Drosophila DmGluRA is required for social interaction and memory.Frontiers in pharmacology · 2013Article
- UsingDrug discovery today. Technologies · 2012Article
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2 authors.
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Abstract
A current hypothesis proposes that fragile X mental retardation protein (FMRP), an RNA-binding translational regulator, acts downstream of glutamatergic transmission, via metabotropic glutamate receptor (mGluR) G(q)-dependent signaling, to modulate protein synthesis critical for trafficking ionotropic glutamate receptors (iGluRs) at synapses. However, direct evidence linking FMRP and mGluR function with iGluR synaptic expression is limited. In this study, we use the Drosophila fragile X model to test this hypothesis at the well characterized glutamatergic neuromuscular junction (NMJ). Two iGluR classes reside at this synapse, each containing common GluRIIC (III), IID and IIE subunits, and variable GluRIIA (A-class) or GluRIIB (B-class) subunits. In Drosophila fragile X mental retardation 1 (dfmr1) null mutants, A-class GluRs accumulate and B-class GluRs are lost, whereas total GluR levels do not change, resulting in a striking change in GluR subclass ratio at individual synapses. The sole Drosophila mGluR, DmGluRA, is also expressed at the NMJ. In dmGluRA null mutants, both iGluR classes increase, resulting in an increase in total synaptic GluR content at individual synapses. Targeted postsynaptic dmGluRA overexpression causes the exact opposite GluR phenotype to the dfmr1 null, confirming postsynaptic GluR subtype-specific regulation. In dfmr1; dmGluRA double null mutants, there is an additive increase in A-class GluRs, and a similar additive impact on B-class GluRs, toward normal levels in the double mutants. These results show that both dFMRP and DmGluRA differentially regulate the abundance of different GluR subclasses in a convergent mechanism within individual postsynaptic domains.
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