Search results for " X-Linked"

showing 10 items of 37 documents

De novo mutations in the X-linked TFE3 gene cause intellectual disability with pigmentary mosaicism and storage disorder-like features

2020

IntroductionPigmentary mosaicism (PM) manifests by pigmentation anomalies along Blaschko’s lines and represents a clue toward the molecular diagnosis of syndromic intellectual disability (ID). Together with new insights on the role for lysosomal signalling in embryonic stem cell differentiation, mutations in the X-linked transcription factor 3 (TFE3) have recently been reported in five patients. Functional analysis suggested these mutations to result in ectopic nuclear gain of functions.Materials and methodsSubsequent data sharing allowed the clustering of de novo TFE3 variants identified by exome sequencing on DNA extracted from leucocytes in patients referred for syndromic ID with or with…

0301 basic medicineMESH: Basic Helix-Loop-Helix Leucine Zipper Transcription Factors[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyIntellectual disabilityTFE3Biology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsMESH: Intellectual Disability03 medical and health sciencesExon0302 clinical medicineMESH: Whole Exome SequencingMESH: ChildIntellectual disabilityGeneticsmedicineMissense mutationGeneGenetics (clinical)Exome sequencingPigmentary mosaicismMESH: Pathology MolecularGeneticsMESH: AdolescentMESH: HumansAlternative splicingLysosomal metabolismMESH: Child Preschool[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyMESH: Adultmedicine.diseasePhenotypeMESH: InfantMESH: MaleTFE3Storage disorder030104 developmental biologyMESH: Genes X-Linked[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMESH: Young AdultMESH: EpilepsyMESH: MosaicismMESH: Pigmentation DisordersMESH: Female030217 neurology & neurosurgery
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Expanding the Phenotype Associated with NAA10-Related N-Terminal Acetylation Deficiency

2016

International audience; N-terminal acetylation is a common protein modification in eukaryotes associated with numerous cellular processes. Inherited mutations in NAA10, encoding the catalytic subunit of the major N-terminal acetylation complex NatA have been associated with diverse, syndromic X-linked recessive disorders, whereas de novo missense mutations have been reported in one male and one female individual with severe intellectual disability but otherwise unspecific phenotypes. Thus, the full genetic and clinical spectrum of NAA10 deficiency is yet to be delineated. We identified three different novel and one known missense mutation in NAA10, de novo in 11 females, and due to maternal…

0301 basic medicineMaleModels MolecularMicrocephalyMutation MissenseBiologyGermlineKEY WORDS: NAA1003 medical and health sciencesGermline mutationGenes X-LinkedIntellectual disabilityGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseN-Terminal Acetyltransferase EGenetics (clinical)Genetic Association StudiesGerm-Line MutationN-Terminal Acetyltransferase AResearch ArticlesGeneticsX-linked[SDV.GEN]Life Sciences [q-bio]/GeneticsRegional Council of BurgundyMosaicismN-terminal acetylationAcetylationmedicine.diseasePhenotypePedigreeOgden SyndromeX‐linked030104 developmental biologyNAA10intellectual disabilityN‐terminal acetylationContract grant sponsors: Dijon University HospitalFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsNAA15Research ArticleHuman Mutation
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Large national series of patients with Xq28 duplication involving MECP2: Delineation of brain MRI abnormalities in 30 affected patients.

2016

International audience; Xq28 duplications encompassing MECP2 have been described in male patients with a severe neurodevelopmental disorder associated with hypotonia and spasticity, severe learning disability, stereotyped movements, and recurrent pulmonary infections. We report on standardized brain magnetic resonance imaging (MRI) data of 30 affected patients carrying an Xq28 duplication involving MECP2 of various sizes (228 kb to 11.7 Mb). The aim of this study was to seek recurrent malformations and attempt to determine whether variations in imaging features could be explained by differences in the size of the duplications. We showed that 93% of patients had brain MRI abnormalities such …

0301 basic medicineMalePathologyMethyl-CpG-Binding Protein 2[SDV]Life Sciences [q-bio]030105 genetics & heredityCorpus callosumLateral ventricles0302 clinical medicineGene DuplicationIKBKGFLNAChildGenetics (clinical)GeneticsBrain Diseasesmedicine.diagnostic_testMiddle AgedPrognosisMagnetic Resonance ImagingHypotonia3. Good healthPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structurePhenotypeXq28 duplicationChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentGenotypeBiologygenotype-phenotype correlationWhite matter03 medical and health sciencesYoung AdultGeneticsmedicineHumansGenetic Association StudiesChromosomes Human X[ SDV ] Life Sciences [q-bio]Infant NewbornInfantMagnetic resonance imagingHyperintensitynervous system diseasesMental Retardation X-LinkedMECP2 gene030217 neurology & neurosurgeryAmerican journal of medical genetics. Part A
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Further delineation of the female phenotype with KDM5C disease causing variants: 19 new individuals and review of the literature.

2020

X-linked intellectual disability (XLID) is a genetically heterogeneous condition involving more than 100 genes. To date, 35 pathogenic variants have been reported in the lysine specific demethylase 5C (KDM5C) gene. KDM5C variants are one of the major causes of moderate to severe XLID. Affected males present with short stature, distinctive facial features, behavioral disorders, epilepsy, and spasticity. For most of these variants, related female carriers have been reported, but phenotypic descriptions were poor. Here, we present clinical and molecular features of 19 females carrying 10 novel heterozygous variants affecting KDM5C function, including five probands with de novo variants. Four h…

0301 basic medicineProbandAdultMaleHeterozygoteX-linked intellectual disabilityGenetic counselingDisease030105 genetics & heredityBiologyShort stature03 medical and health sciencesYoung AdultGenes X-LinkedIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumans10. No inequalityExomeGenetics (clinical)GeneticsHistone DemethylasesEpilepsyGenetic heterogeneityGenetic Variationmedicine.disease3. Good health030104 developmental biologyPhenotypeChild PreschoolMental Retardation X-LinkedFemalemedicine.symptomClinical geneticsREFERENCES
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Expanding the clinical phenotype of patients with a ZDHHC9 mutation.

2013

In 2007, 250 families with X-linked intellectual disability (XLID) were screened for mutations in genes on the X-chromosome, and in 4 of these families, mutations in the ZDHHC9 gene were identified. The ID was either isolated or associated with a marfanoid habitus. ZDHHC9 encodes a palmitoyl transferase that catalyzes the posttranslational modification of NRAS and HRAS. Since this first description, no additional patient with a ZDHHC9 mutation has been reported in the literature. Here, we describe a large family in which we identified a novel pathogenic ZDHHC9 nonsense mutation (p.Arg298*) by parallel sequencing of all X-chromosome exons. The mutation cosegregated with the clinical phenotyp…

AdultMaleAdolescentX-linked intellectual disabilityGenetic counselingNonsense mutationNeuropsychological TestsBioinformaticsYoung AdultFatal OutcomeGenes X-LinkedIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansHRASChildGenetics (clinical)GeneticsMassive parallel sequencingAcrocyanosisbusiness.industryBrainFaciesmedicine.diseaseMagnetic Resonance ImagingPedigreePhenotypeMutation (genetic algorithm)MutationbusinessAcyltransferasesAmerican journal of medical genetics. Part A
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Oligophrenin 1 mutations frequently cause X-linked mental retardation with cerebellar hypoplasia

2005

Background: Mutations of oligophrenin 1, one of the first genes identified in nonspecific X-linked mental retardation (MRX), have been described in patients with moderate to severe cognitive impairment and predominant cerebellar hypoplasia, in the vermis. Objective: To further delineate the phenotypic and mutational spectrum of the syndrome, by screening oligophrenin 1 in two cohorts of male patients with mental retardation (MR) with or without known posterior fossa anomalies. Methods: Clinical examination, cognitive testing, MRI studies, and mutational analysis (denaturing gradient gel electrophoresis and direct sequencing) on blood lymphocytes were performed in 213 unrelated affected indi…

AdultMaleCerebellumAdolescentGenotypeDNA Mutational AnalysisNonsense mutationNervous System Malformationsmedicine.disease_causeCohort StudiesExonCerebellar DiseasesCerebellummedicineHumansGenetic TestingChildCerebellar hypoplasiaGeneticsMutationSplice site mutationGTPase-Activating ProteinsNuclear Proteinsmedicine.diseaseMagnetic Resonance ImagingHypoplasiaPedigreeDevelopmental disorderAlternative SplicingCytoskeletal ProteinsPhenotypemedicine.anatomical_structureFacial AsymmetryCodon NonsenseChild PreschoolMutationMental Retardation X-LinkedRNA Splice SitesNeurology (clinical)PsychologyGene DeletionNeurology
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Four unrelated patients with lubs X-linked mental retardation syndrome and different Xq28 duplications

2010

The Lubs X-linked mental retardation syndrome (MRXSL) is caused by small interstitial duplications at distal Xq28 including the MECP2 gene. Here we report on four novel male patients with MRXSL and different Xq28 duplications delineated by microarray-based chromosome analysis. All mothers were healthy carriers of the duplications. Consistent with an earlier report [Bauters et al. (2008); Genome Res 18: 847-858], the distal breakpoints of all four Xq28 duplications were located in regions containing low-copy repeats (LCRs; J, K, and L groups), which may facilitate chromosome breakage and reunion events. The proximal breakpoint regions did not contain known LCRs. Interestingly, we identified …

AdultMaleHeterozygoteBotulinum ToxinsAdolescentMethyl-CpG-Binding Protein 2MECP2 duplication syndromeMothersBiologyMECP2Gene duplicationGeneticsmedicineHumansChildGenetics (clinical)X chromosomeMuscle contractureChromosome AberrationsGeneticsChromosomes Human XBreakpointInfantmedicine.diseasePedigreeXq28Child PreschoolMental Retardation X-LinkedFemaleChromosome breakageAmerican Journal of Medical Genetics Part A
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A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation.

2007

X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with …

AdultMaleMicrocephalycongenital hereditary and neonatal diseases and abnormalitiesGermline mosaicismLocus (genetics)BiologyMicrophthalmiaFrameshift mutationGenetic linkageGenes X-LinkedIntellectual DisabilityGeneticsmedicineMissense mutationHumansMicrophthalmosAbnormalities MultipleFrameshift MutationGenetics (clinical)GeneticsChromosomes Human XNuclear ProteinsGenetic Diseases X-LinkedSyndromemedicine.diseasePedigreeLenz microphthalmia syndromeDNA-Binding ProteinsChild PreschoolMicrocephalyFemaleCarrier ProteinsGene DeletionEuropean journal of human genetics : EJHG
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A female with X‐linked Nephrogenic diabetes insipidus in a family with inherited central diabetes Insipidus: Case report and review of the literature

2020

There are two forms of diabetes insipidus, central (neurohypophyseal), and nephrogenic, caused by pathogenic variants in the AVP gene and the AVPR2 or AQP2 genes, respectively. We report on a four-generation family, seven individuals had central diabetes insipidus (CDI) and the female index patient seen from age 16 to 26 years had (mild) nephrogenic diabetes insipidus. In her father with CDI, a known pathogenic heterozygous AVP variant c.232_234del p.(Glu78del) was identified, confirming the diagnosis of CDI in him and the other affected family members. In the proband, molecular analysis disclosed a novel heterozygous AVPR2 gene variant, c.962A > T p.(Asn321Ile) and an extremely skewed X-in…

AdultMaleProbandReceptors Vasopressinmedicine.medical_specialtyAdolescentVasopressinsMutation Missense610 MedizinDiabetes Insipidus NephrogenicYoung AdultGenes X-LinkedX Chromosome Inactivation610 Medical sciencesInternal medicineArginine vasopressin receptor 2Exome SequencingDiabetes MellitusGeneticsmedicineHumansMissense mutationProtein PrecursorsGenetics (clinical)Exome sequencingNeurophysinsAquaporin 2business.industryHeterozygote advantagemedicine.diseaseNephrogenic diabetes insipidusPedigreeDiabetes Insipidus NeurogenicEndocrinologyAquaporin 2Diabetes insipidusFemalebusinessAmerican Journal of Medical Genetics Part A
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Influence of sex and genetic variability on expression of X-linked genes in human monocytes

2011

Abstract In humans, the fraction of X-linked genes with higher expression in females has been estimated to be 5% from microarray studies, a proportion lower than the 25% of genes thought to escape X inactivation. We analyzed 715 X-linked transcripts in circulating monocytes from 1,467 subjects and found an excess of female-biased transcripts on the X compared to autosomes (9.4% vs 5.5%, p  −5 ). Among the genes not previously known to escape inactivation, the most significant one was EFHC2 whose 20% of variability was explained by sex. We also investigated cis expression quantitative trait loci (eQTLs) by analyzing 15,703 X-linked SNPs. The frequency and magnitude of X-linked cis eQTLs were…

AdultMaleTranscription GeneticMicroarrayQuantitative Trait LociSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideMonocytesX-inactivationSex FactorsGenes X-LinkedX Chromosome InactivationGene expressionGeneticsHumansGenetic variabilityGeneAgedGeneticsChromosomes Human XAutosomeCalcium-Binding ProteinsGenderGenetic VariationMiddle AgedExpression Quantitative Trait LocusExpression quantitative trait lociFemaleGene expressionGenome-Wide Association StudyGenomics
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