ArticleProceedings of the National Academy of Sciences of the United States of America2007
Fragile X mental retardation protein FMRP and the RNA export factor NXF2 associate with and destabilize Nxf1 mRNA in neuronal cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 84 citations in OpenAlex.
- Division of labor in trypanosome RNA processing and export through expanded Mex67 paralogs.Nucleic acids research · 2026Article
- Mitochondrial dysfunction in Fragile X syndrome and Fragile X-associated tremor/ataxia syndrome: prospect use of antioxidants and mitochondrial nutrients.Molecular biology reports · 2024Review
- Identification and Analysis of ZIC-Related Genes in Cerebellum of Autism Spectrum Disorders.Neuropsychiatric disease and treatment · 2024Article
- Blockade of Type 2A Protein Phosphatase Signaling Attenuates Complement C1q-Mediated Microglial Phagocytosis of Glutamatergic Synapses Induced by Amyloid Fibrils.Molecular neurobiology · 2023Article
- Progranulin is an FMRP target that influences macroorchidism but not behaviour in a mouse model of Fragile X Syndrome.Current research in neurobiology · 2023Article
- Sending the message: specialized RNA export mechanisms in trypanosomes.Trends in parasitology · 2022Review
- Local mRNA translation and cytoskeletal reorganization: Mechanisms that tune neuronal responses.Frontiers in molecular neuroscience · 2022Review
- Article
- Mammalian Neuronal mRNA Transport Complexes: The Few Knowns and the Many Unknowns.Frontiers in integrative neuroscience · 2021Review
- Cataloguing and Selection of mRNAs Localized to Dendrites in Neurons and Regulated by RNA-Binding Proteins in RNA Granules.Biomolecules · 2020Review
- Activation of mGluR1 Mediates C1q-Dependent Microglial Phagocytosis of Glutamatergic Synapses in Alzheimer's Rodent Models.Molecular neurobiology · 2019Article
- Review
- Review
- The Fragile X Protein and Genome Function.Molecular neurobiology · 2019Review
- Fragile X mental retardation protein modulates the stability of its m6A-marked messenger RNA targets.Human molecular genetics · 2018Article
- The fragile X mental retardation protein regulates tumor invasiveness-related pathways in melanoma cells.Cell death & disease · 2017Article
- SR proteins: To shuttle or not to shuttle, that is the question.The Journal of cell biology · 2017Article
- An NXF1 mRNA with a retained intron is expressed in hippocampal and neocortical neurons and is translated into a protein that functions as an Nxf1 cofactor.Molecular biology of the cell · 2016Article
- Cytoplasmic localization of SBR (Dm NXF1) protein and its zonal distribution in the ganglia of Drosophila melanogaster larvae.Invertebrate neuroscience : IN · 2016Article
- Luzp4 defines a new mRNA export pathway in cancer cells.Nucleic acids research · 2015Article
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fragile X syndrome is caused by the inactivation of the X-linked FMR1 gene, leading to the loss of its encoded protein FMRP. Although macroorchidism and defects in neuronal architecture and function have been associated with lack of FMRP, the exact molecular mechanism underlying this disease remains unclear. We have reported previously that in the brain and testis of mice, FMRP specifically interacts with a distinct mRNA nuclear export factor NXF2 but not with its close relative NXF1, a ubiquitously expressed essential mRNA nuclear export factor. This interaction marked NXF2 as a putative functional partner of FMRP. Here, we demonstrate by immunoprecipitation and quantitative real-time RT-PCR that, in cultured mouse neuronal cells, both FMRP and NXF2 are present in Nxf1 mRNA-containing ribonucleoprotein particles. Further, we show that expression of NXF2 leads to the destabilization of Nxf1 mRNA and that this effect is abolished when Fmr1 expression is reduced by siRNA, arguing that both proteins collaborate to exert this effect. Importantly, these findings correlate well with our observations that in both mouse hippocampal neurons and male germ cells where the expression of FMRP and NXF2 is most prominent, the expression of NXF1 is relatively poorly expressed. Our studies thus identify Nxf1 mRNA as a likely biologically relevant in vivo target of both FMRP and NXF2 and implicate FMRP, in conjunction with NXF2, as a posttranscriptional regulator of a major mRNA export factor. Such regulation may prove important in the normal development and function of neurons as well as of male germ cells.
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