Search results for "FMR1"

showing 9 items of 9 documents

Enhanced Prefrontal Neuronal Activity and Social Dominance Behavior in Postnatal Forebrain Excitatory Neuron-Specific Cyfip2 Knock-Out Mice

2020

The cytoplasmic fragile X mental retardation 1 (FMR1)-interacting protein 2 (CYFIP2) gene is associated with epilepsy, intellectual disability (ID), and developmental delay, suggesting its critical role in proper neuronal development and function. CYFIP2 is involved in regulating cellular actin dynamics and also interacts with RNA-binding proteins. However, the adult brain function of CYFIP2 remains unclear because investigations thus far are limited to Cyfip2 heterozygous (Cyfip2+/- ) mice owing to the perinatal lethality of Cyfip2-null mice. Therefore, we generated Cyfip2 conditional knock-out (cKO) mice with reduced CYFIP2 expression in postnatal forebrain excitatory neurons (CaMKIIα-Cre…

0301 basic medicineDendritic spinesocial dominanceBiologyFilamentous actinneuronal activitylcsh:RC321-57103 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineexcitabilityCYFIP2Premovement neuronal activityPrefrontal cortexlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyBrief Research ReportFMR1030104 developmental biologyKnockout mouseForebrainExcitatory postsynaptic potentialNeurosciencemedial prefrontal cortex030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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Dysregulated Prefrontal Cortex Inhibition in Prepubescent and Adolescent Fragile X Mouse Model

2020

Changes in excitation and inhibition are associated with the pathobiology of neurodevelopmental disorders of intellectual disability and autism and are widely described in Fragile X syndrome (FXS). In the prefrontal cortex (PFC), essential for cognitive processing, excitatory connectivity and plasticity are found altered in the FXS mouse model, however, little is known about the state of inhibition. To that end, we investigated GABAergic signaling in the Fragile X Mental Retardation 1 (FMR1) knock out (Fmr1-KO) mouse medial PFC (mPFC). We report changes at the molecular, and functional levels of inhibition at three (prepubescence) and six (adolescence) postnatal weeks. Functional changes we…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesGABAB receptorBiologyInhibitory postsynaptic potentiallcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceGABA0302 clinical medicineNeurodevelopmental disorderSDG 3 - Good Health and Well-beingmedicinePrefrontal cortexMolecular Biologylcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal Researchprefrontal cortexGABAA receptormedicine.diseaseelectrophysiologyFMR1Fragile X syndrome030104 developmental biologyplasticityFragile XGABAergic/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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Neuroactive Steroids Reverse Tonic Inhibitory Deficits in Fragile X Syndrome Mouse Model

2018

Fragile X syndrome (FXS) is the most common form of inherited intellectual disability. A reduction in neuronal inhibition mediated by γ-aminobutyric acid type A receptors (GABAARs) has been implicated in the pathophysiology of FXS. Neuroactive steroids (NASs) are known allosteric modulators of GABAAR channel function, but recent studies from our laboratory have revealed that NASs also exert persistent metabotropic effects on the efficacy of tonic inhibition by increasing the protein kinase C (PKC)-mediated phosphorylation of the α4 and β3 subunits which increase the membrane expression and boosts tonic inhibition. We have assessed the GABAergic signaling in the hippocampus of fragile X ment…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyNeuroactive steroidGABAA receptor (GABAAR)fragile XInhibitory postsynaptic potentialTonic (physiology)lcsh:RC321-571tonic inhibition03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineInternal medicinemedicineMolecular Biologylcsh:Neurosciences. Biological psychiatry. NeuropsychiatryProtein kinase COriginal ResearchChemistryphosphorylationDentate gyrusFMR1030104 developmental biologyEndocrinologyMetabotropic receptorGABAergicneurosteroidbenzodiazepine030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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Criss‐crossing autism spectrum disorder and adult neurogenesis

2021

Autism spectrum disorder (ASD) comprises a group of multifactorial neurodevelopmental disorders primarily characterized by deficits in social interaction and repetitive behavior. Although the onset is typically in early childhood, ASD poses a lifelong challenge for both patients and caretakers. Adult neurogenesis (AN) is the process by which new functional neurons are created from neural stem cells existing in the post-natal brain. The entire event is based on a sequence of cellular processes, such as proliferation, specification of cell fate, maturation, and ultimately, synaptic integration into the existing neural circuits. Hence, AN is implicated in structural and functional brain plasti…

AdultAutism Spectrum DisorderNeurogenesisNeurogenesisCell fate determinationBiologymedicine.diseaseAffect (psychology)BiochemistryFMR1Neural stem cellCellular and Molecular NeuroscienceNeural Stem CellsNeurodevelopmental DisordersAutism spectrum disorderChild Preschoolmental disordersmedicineBiological neural networkAnimalsHumansEarly childhoodNeuroscienceJournal of Neurochemistry
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Intragenic FMR1 disease-causing variants: a significant mutational mechanism leading to Fragile-X syndrome

2017

International audience; Fragile-X syndrome (FXS) is a frequent genetic form of intellectual disability (ID). The main recurrent mutagenic mechanism causing FXS is the expansion of a CGG repeat sequence in the 5'-UTR of the FMR1 gene, therefore, routinely tested in ID patients. We report here three FMR1 intragenic pathogenic variants not affecting this sequence, identified using high-throughput sequencing (HTS): a previously reported hemizygous deletion encompassing the last exon of FMR1, too small to be detected by array-CGH and inducing decreased expression of a truncated form of FMRP protein, in three brothers with ID (family 1) and two splice variants in boys with sporadic ID: a de novo …

Male0301 basic medicinemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesdiagnosisRNA SplicingBiologymedicine.disease_causePolymorphism Single NucleotideArticleFragile X Mental Retardation Protein03 medical and health sciencesExonGenetic linkageplacebo-controlled trial[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansgeneGenetics (clinical)GeneticsMutationintron 10SiblingsMiddle Agedmedicine.diseaseFMR1Human genetics3. Good healthFragile X syndromedevelopmental delayof-the-literature030104 developmental biologyintellectual disabilityFragile X SyndromeMutationmental-retardationMedical geneticsFemalepoint mutationdouble-blind[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Recurrent missense variant in the nuclear export signal of FMR1 associated with FXS-like phenotype including intellectual disability, ASD, facial abn…

2021

Fragile X syndrome (FXS; MIM 300624) is an X-linked genetic disorder characterized by physical abnormalities associated with intellectual disability and a wide spectrum of neurological and psychiatric impairments. FXS occurs more frequently in males, 1 in 5000 males and 1 in 8000 females accounting for 1-2% of overall intellectual disability (ID). In more than 99% of patients, FXS results from expansions of a CGG triplet repeat (>200 in male) of the FMR1 gene. In the last years an increasing number, albeit still limited, of FXS subjects carrying FMR1 mutations including deletions, splicing errors, missense, and nonsense variants was reported. Nevertheless, the studies concerning the func…

MaleNuclear Export SignalsSettore M-PSI/02 - Psicobiologia E Psicologia FisiologicaAutism Spectrum DisorderMutation MissenseGeneral MedicineFMR1 point mutationSettore MED/39 - Neuropsichiatria InfantileFragile X Mental Retardation ProteinPhenotypeSettore MED/38 - Pediatria Generale E SpecialisticaIntellectual DisabilityAutism spectrum disorders ASDSettore M-PSI/08 - Psicologia ClinicaGeneticsHumansIntellectual disability IDFemaleNuclear export signal NES.Genetics (clinical)Fragile X syndrome
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Xq27 FRAXA Locus is a Strong Candidate for Dyslexia: Evidence from a Genome-Wide Scan in French Families

2012

Dyslexia is a frequent neurodevelopmental learning disorder. To date, nine susceptibility loci have been identified, one of them being DYX9, located in Xq27. We performed the first French SNP linkage study followed by candidate gene investigation in dyslexia by studying 12 multiplex families (58 subjects) with at least two children affected, according to categorical restrictive criteria for phenotype definition. Significant results emerged on Xq27.3 within DYX9. The maximum multipoint LOD score reached 3,884 between rs12558359 and rs454992. Within this region, seven candidate genes were investigated for mutations in exonic sequences (CXORF1, CXORF51, SLITRK2, FMR1, FMR2, ASFMR1, FMR1NB), al…

Malecongenital hereditary and neonatal diseases and abnormalitiesCandidate geneGenotypeGenome-wide association studyLocus (genetics)BiologyPolymorphism Single NucleotideGenomeDyslexiaFragile X Mental Retardation ProteinGenes X-LinkedGenotypeGeneticsmedicineHumansSNPGenetic Predisposition to DiseaseChildGenetics (clinical)Ecology Evolution Behavior and SystematicsGeneticsChromosomes Human XDyslexiamedicine.diseaseFMR1Settore MED/39 - Neuropsichiatria InfantilePedigreeGenetic LociFemaleFranceDyslexia Linkage study Multiplex families Fmr1 Dyx 9 loci InLod ScoreGenome-Wide Association StudyBehavior Genetics
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Ythdf is a N6‐methyladenosine reader that modulates Fmr1 target mRNA selection and restricts axonal growth in Drosophila

2021

Abstract N6‐methyladenosine (m6A) regulates a variety of physiological processes through modulation of RNA metabolism. This modification is particularly enriched in the nervous system of several species, and its dysregulation has been associated with neurodevelopmental defects and neural dysfunctions. In Drosophila, loss of m6A alters fly behavior, albeit the underlying molecular mechanism and the role of m6A during nervous system development have remained elusive. Here we find that impairment of the m6A pathway leads to axonal overgrowth and misguidance at larval neuromuscular junctions as well as in the adult mushroom bodies. We identify Ythdf as the main m6A reader in the nervous system,…

Nervous systemCancer ResearchAdenosineMessengerRNA-binding proteinBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyFragile X Mental Retardation Protein03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsDrosophila ProteinsFmr1; RNA modification; Ythdf; m6A; nervous systemRNA MessengerFmr1Molecular BiologyDrosophila030304 developmental biologyNeurons0303 health sciencesGeneral Immunology and MicrobiologyProteomics and Chromatin BiologyGeneral Neurosciencenervous systemRNA-Binding ProteinsTranslation (biology)Articlesm6AProtein Biosynthesis & Quality ControlRNA modificationYthdfbiology.organism_classificationRNA BiologyFMR1Fmr1; RNA modification; Ythdf; m6A; nervous system; Adenosine; Animals; Axons; Drosophila Proteins; Drosophila melanogaster; Fragile X Mental Retardation Protein; Neurons; RNA Messenger; RNA-Binding ProteinsAxonsCell biologyDrosophila melanogastermedicine.anatomical_structurechemistryMushroom bodiesRNATarget mrnaN6-Methyladenosine030217 neurology & neurosurgeryNeuroscienceThe EMBO Journal
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Cognitive Deficits and Associated ERP N400 Abnormalities in FXTAS With Parkinsonism

2018

Objective: To examine cognitive deficits and associated brain activity in fragile X-associated tremor/ataxia syndrome (FXTAS) patients with parkinsonism (FXTp+), in relation to FXTAS patients without parkinsonism (FXTp-), and normal elderly controls (NC). Methods: Retrospective reviews were performed in 65 FXTAS patients who participated in the event-related brain potential (ERP) study and also had either a videotaped neurological examination or a neurological examination for extrapyramidal signs. Parkinsonism was defined as having bradykinesia with at least one of the following: rest tremor, postural instability, hypermyotonia, or rigidity. Eleven FXTp+ patients were identified and compare…

cognition0301 basic medicineAgingmedicine.medical_specialtyAtaxialcsh:QH426-470Clinical SciencesNeurodegenerativeAudiologysemantic processingVerbal learningBasic Behavioral and Social Science03 medical and health sciencesRare Diseasesevent-related potential0302 clinical medicineClinical ResearchBehavioral and Social ScienceGeneticsmedicine2.1 Biological and endogenous factorsAetiologyLate positive componentparkinsonismGenetics (clinical)Original ResearchParkinson's DiseaseCalifornia Verbal Learning Testbusiness.industryParkinsonismNeurosciencesevent-related potential (ERP)medicine.diseaseFMR1Brain Disorderslcsh:Genetics030104 developmental biologyNeurologicalMolecular MedicineMental healthmedicine.symptomVerbal memorybusinessFMR1 premutationLaw030217 neurology & neurosurgeryExecutive dysfunctionFrontiers in Genetics
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