ArticleNature neuroscience2011
Modulation of dADAR-dependent RNA editing by the Drosophila fragile X mental retardation protein.
Article in Nature neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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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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Who cites it
59 citing papers in PubMed, 86 citations in OpenAlex.
- The role of RNA binding proteins in cancer biology: A focus on FMRP.Genes & diseases · 2025Review
- Review
- FMR1 genetically interacts with DISC1 to regulate glutamatergic synaptogenesis.Schizophrenia (Heidelberg, Germany) · 2024Article
- RNA modifications in physiology and disease: towards clinical applications.Nature reviews. Genetics · 2024Review
- The multifaceted role of Fragile X-Related Protein 1 (FXR1) in cellular processes: an updated review on cancer and clinical applications.Cell death & disease · 2024Review
- Overview: Research on the Genetic Architecture of the Developing Cerebral Cortex in Norms and Diseases.Methods in molecular biology (Clifton, N.J.) · 2024Article
- The Fragile X Protein Family in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2023Review
- ADAR2 enzymes: efficient site-specific RNA editors with gene therapy aspirations.RNA (New York, N.Y.) · 2022Review
- Epitranscriptomic dynamics in brain development and disease.Molecular psychiatry · 2022Review
- RNA and neuronal function: the importance of post-transcriptional regulation.Oxford open neuroscience · 2022Review
- 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
- RNA Modifications and RNA Metabolism in Neurological Disease Pathogenesis.International journal of molecular sciences · 2021Review
- Review
- Article
- An "Omic" Overview of Fragile X Syndrome.Biology · 2021Review
- The molecular biology of FMRP: new insights into fragile X syndrome.Nature reviews. Neuroscience · 2021Review
- The Fine Art of Writing a Message: RNA Metabolism in the Shaping and Remodeling of the Nervous System.Frontiers in molecular neuroscience · 2021Review
- Zinc Finger RNA-Binding Protein Zn72D Regulates ADAR-Mediated RNA Editing in Neurons.Cell reports · 2020Article
- Bi-allelic ADARB1 Variants Associated with Microcephaly, Intellectual Disability, and Seizures.American journal of human genetics · 2020Article
- Membrane and synaptic defects leading to neurodegeneration in Adar mutant Drosophila are rescued by increased autophagy.BMC biology · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Loss of FMR1 gene function results in fragile X syndrome, the most common heritable form of intellectual disability. The protein encoded by this locus (FMRP) is an RNA-binding protein that is thought to primarily act as a translational regulator; however, recent studies have implicated FMRP in other mechanisms of gene regulation. We found that the Drosophila fragile X homolog (dFMR1) biochemically interacted with the adenosine-to-inosine RNA-editing enzyme dADAR. Adar and Fmr1 mutant larvae exhibited distinct morphological neuromuscular junction (NMJ) defects. Epistasis experiments based on these phenotypic differences revealed that Adar acts downstream of Fmr1 and that dFMR1 modulates dADAR activity. Furthermore, sequence analyses revealed that a loss or overexpression of dFMR1 affects editing efficiency on certain dADAR targets with defined roles in synaptic transmission. These results link dFMR1 with the RNA-editing pathway and suggest that proper NMJ synaptic architecture requires modulation of dADAR activity by dFMR1.
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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.