ArticleProceedings of the National Academy of Sciences of the United States of America2016
Fragile X Mental Retardation Protein (FMRP) controls diacylglycerol kinase activity in neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 100 citations in OpenAlex.
- Genome-wide profiling of RNA 2'-O-methylation in neurons and identification of orphan snoRNA targets.Research square · 2026Article
- Modulators of Diacylglycerol Kinase Activity: A Review of Advances and Challenges.Medicinal research reviews · 2026Review
- Genome-wide profiling of RNA 2'-bioRxiv : the preprint server for biology · 2025Article
- Designing New Natural-Mimetic Phosphatidic Acid: A Versatile and Innovative Synthetic Strategy for Glycerophospholipid Research.Angewandte Chemie (International ed. in English) · 2025Article
- From Discovery to Innovative Translational Approaches in 80 Years of Fragile X Syndrome Research.Biomedicines · 2025Review
- Diacylglycerol Kinases and Its Role in Lipid Metabolism and Related Diseases.International journal of molecular sciences · 2024Review
- State-of-the-art therapies for fragile X syndrome.Developmental medicine and child neurology · 2024Review
- EZH2 inhibition reactivates epigenetically silencedFrontiers in neuroscience · 2024Article
- FMRP Enhances the Translation ofInternational journal of molecular sciences · 2023Article
- Deregulation of ER-mitochondria contact formation and mitochondrial calcium homeostasis mediated by VDAC in fragile X syndrome.Developmental cell · 2023Article
- The activation of mGluR4 rescues parallel fiber synaptic transmission and LTP, motor learning and social behavior in a mouse model of Fragile X Syndrome.Molecular autism · 2023Article
- Astrocytes in fragile X syndrome.Frontiers in cellular neuroscience · 2023Review
- Investigating cell-specific effects of FMRP deficiency on spiny projection neurons in a mouse model of Fragile X syndrome.Frontiers in cellular neuroscience · 2023Article
- Integrative omics indicate FMRP sequesters mRNA from translation and deadenylation in human neuronal cells.Molecular cell · 2022Article
- Article
- AAV-delivered diacylglycerol kinase DGKk achieves long-term rescue of fragile X syndrome mouse model.EMBO molecular medicine · 2022Article
- Review
- Phylogenetic and Molecular Analyses Identify SNORD116 Targets Involved in the Prader-Willi Syndrome.Molecular biology and evolution · 2022Article
- Combining affinity purification and mass spectrometry to define the network of the nuclear proteins interacting with the N-terminal region of FMRP.Frontiers in molecular biosciences · 2022Article
- Axonal mRNA localization and local translation in neurodegenerative disease.Neural regeneration research · 2021Review
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Authors and funding
17 authors at 11 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fragile X syndrome (FXS) is caused by the absence of the Fragile X Mental Retardation Protein (FMRP) in neurons. In the mouse, the lack of FMRP is associated with an excessive translation of hundreds of neuronal proteins, notably including postsynaptic proteins. This local protein synthesis deregulation is proposed to underlie the observed defects of glutamatergic synapse maturation and function and to affect preferentially the hundreds of mRNA species that were reported to bind to FMRP. How FMRP impacts synaptic protein translation and which mRNAs are most important for the pathology remain unclear. Here we show by cross-linking immunoprecipitation in cortical neurons that FMRP is mostly associated with one unique mRNA: diacylglycerol kinase kappa (Dgkκ), a master regulator that controls the switch between diacylglycerol and phosphatidic acid signaling pathways. The absence of FMRP in neurons abolishes group 1 metabotropic glutamate receptor-dependent DGK activity combined with a loss of Dgkκ expression. The reduction of Dgkκ in neurons is sufficient to cause dendritic spine abnormalities, synaptic plasticity alterations, and behavior disorders similar to those observed in the FXS mouse model. Overexpression of Dgkκ in neurons is able to rescue the dendritic spine defects of the Fragile X Mental Retardation 1 gene KO neurons. Together, these data suggest that Dgkκ deregulation contributes to FXS pathology and support a model where FMRP, by controlling the translation of Dgkκ, indirectly controls synaptic proteins translation and membrane properties by impacting lipid signaling in dendritic spine.
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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.