Search results for "imprint"

showing 10 items of 194 documents

Genome-wide associations for birth weight and correlations with adult disease

2016

Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW (P < 5 × 10(-8)). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genet…

Male0301 basic medicineNetherlands Twin Register (NTR)AgingDatasets as TopicPhysiologyBlood PressureGenome-wide association studyCoronary Artery DiseaseType 2 diabetesBioinformaticsCHARGE Consortium Hematology Working GroupCohort Studies0302 clinical medicineBirth WeightInsulinGlucose homeostasis030212 general & internal medicineeducation.field_of_studyMultidisciplinaryAnthropometry3. Good healthPhenotype/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleGlycogenSignal TransductionAdulthypertensionGenotypeGeneral Science & TechnologyBirth weightintrauterine growthPopulationQuantitative trait locusBiologyArticlequantitative traitGenomic Imprinting03 medical and health sciencesFetusSDG 3 - Good Health and Well-beingEarly Growth Genetics (EGG) ConsortiumMD MultidisciplinaryGenetic variation/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_medicineHumansmetabolic disordersGenetic Predisposition to DiseaseeducationgenomeGenetic associationGenetic Variationbirth weightta3121Chromatin Assembly and Disassemblymedicine.diseaseta3123Glucose030104 developmental biologyDiabetes Mellitus Type 2Genetic Locigenome-wide association studiesadult diseaseGenome-Wide Association Study
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Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome

2020

Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9pat) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an impri…

Male0301 basic medicinePotassium Channels[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyGeneral Physics and AstronomyDiseasePhenylenediamines[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCraniofacial AbnormalitiesHistonesMice0302 clinical medicineIntellectual disabilityImprinting (psychology)lcsh:ScienceMice KnockoutGeneticsMultidisciplinaryBehavior AnimalbiologyNeurodevelopmental disordersDevelopmental disordersQBrainPhenotypeUp-RegulationPhenotypeHistoneGene Knockdown TechniquesBenzamidesMuscle HypotoniaFemaleLocus CoeruleusEpigeneticsScienceArticleGeneral Biochemistry Genetics and Molecular BiologyGenomic Imprinting03 medical and health sciencesDevelopmental disorders ; Neurodevelopmental disorders ; EpigeneticsIntellectual DisabilitymedicineAnimalsHumansddc:610AlleleGene[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Chemistrymedicine.diseaseHistone Deacetylase InhibitorsMice Inbred C57BLDisease Models Animal030104 developmental biologyAcetylationMutationbiology.proteinlcsh:Q030217 neurology & neurosurgery
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Frequency and characterization of DNA methylation defects in children born SGA

2012

Various genes located at imprinted loci and regulated by epigenetic mechanisms are involved in the control of growth and differentiation. The broad phenotypic variability of imprinting disorders suggests that individuals with inborn errors of imprinting might remain undetected among patients born small for gestational age (SGA). We evaluated quantitative DNA methylation analysis at differentially methylated regions (DMRs) of 10 imprinted loci (PLAGL1, IGF2R DMR2, GRB10, H19 DMR, IGF2, MEG3, NDN, SNRPN, NESP, NESPAS) by bisulphite pyrosequencing in 98 patients born SGA and 50 controls. For IGF2R DMR2, methylation patterns of additional 47 parent pairs and one mother (95 individuals) of patie…

MaleAdolescentMedizinLocus (genetics)BiologyArticleCohort StudiesGenomic ImprintingGeneticsHumansAbnormalities MultipleEpigeneticsImprinting (psychology)ChildGenetics (clinical)MEG3GeneticsFamily HealthInfant NewbornInfantMethylationSequence Analysis DNASyndromeDNA Methylationfemale genital diseases and pregnancy complicationsPedigreeDifferentially methylated regionsPhenotypeGenetic LociChild PreschoolDNA methylationInfant Small for Gestational AgeFemaleGenomic imprinting
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Postnatal loss of Dlk1 imprinting in stem cells and niche astrocytes regulates neurogenesis.

2011

The gene for the atypical NOTCH ligand delta-like homologue 1 (Dlk1) encodes membrane-bound and secreted isoforms that function in several developmental processes in vitro and in vivo. Dlk1, a member of a cluster of imprinted genes, is expressed from the paternally inherited chromosome. Here we show that mice that are deficient in Dlk1 have defects in postnatal neurogenesis in the subventricular zone: a developmental continuum that results in depletion of mature neurons in the olfactory bulb. We show that DLK1 is secreted by niche astrocytes, whereas its membrane-bound isoform is present in neural stem cells (NSCs) and is required for the inductive effect of secreted DLK1 on self-renewal. N…

MaleAgingGenotypeNeurogenesisSubventricular zoneBiologyArticle03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineNeural Stem CellsmedicineAnimalsProtein IsoformsEpigeneticsImprinting (psychology)Stem Cell NicheCells Cultured030304 developmental biologyGenetics0303 health sciencesMultidisciplinaryBase SequenceNeurogenesisCalcium-Binding ProteinsCell MembraneEmbryo MammalianOlfactory BulbNeural stem cellCell biologyMice Inbred C57BLmedicine.anatomical_structureAnimals NewbornAstrocytesDNA methylationNeurogliaIntercellular Signaling Peptides and ProteinsFemaleGenomic imprinting030217 neurology & neurosurgery
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Loss-of-function maternal-effect mutations of PADI6 are associated with familial and sporadic Beckwith-Wiedemann syndrome with multi-locus imprinting…

2020

Abstract Background PADI6 is a component of the subcortical maternal complex, a group of proteins that is abundantly expressed in the oocyte cytoplasm, but is required for the correct development of early embryo. Maternal-effect variants of the subcortical maternal complex proteins are associated with heterogeneous diseases, including female infertility, hydatidiform mole, and imprinting disorders with multi-locus imprinting disturbance. While the involvement of PADI6 in infertility is well demonstrated, its role in imprinting disorders is less well established. Results We have identified by whole-exome sequencing analysis four cases of Beckwith-Wiedemann syndrome with multi-locus imprintin…

MaleBeckwith-Wiedemann SyndromeGenomic imprintingMulti-locus imprinting disturbanceBeckwith–Wiedemann syndromeWhole Exome SequencingProtein-Arginine Deiminase Type 60302 clinical medicinePregnancyImprinting (psychology)ChildGenetics (clinical)Genetics0303 health sciencesDNA methylationPADI6Beckwith-Wiedemann syndrome; DNA methylation; Genomic imprinting; Infertility; Maternal-effect variants; Multi-locus imprinting disturbance; PADI6; Subcortical maternal complex; Adolescent; Adult; Beckwith-Wiedemann Syndrome; Child Preschool; DNA Methylation; Female; Genomic Imprinting; Heterozygote; Humans; Hydatidiform Mole; Infant; Infertility Female; Male; Maternal Inheritance; Mutation; Oocytes; Pedigree; Phenotype; Pregnancy; Protein-Arginine Deiminase Type 6; Siblings; Whole Exome SequencingFemale infertilityMaternal effectHydatidiform MolePedigreePhenotypeChild Preschool030220 oncology & carcinogenesisDNA methylationFemaleMaternal InheritanceInfertility FemaleAdultHeterozygoteAdolescentSubcortical maternal complexBiology03 medical and health sciencesExome SequencingGeneticsmedicineHumansMaternal-effect variantsPreschoolMolecular BiologyLoss function030304 developmental biologyMaternal-effect variantResearchSiblingsInfantmedicine.diseaseHuman geneticsInfertilityMutationOocytesGenomic imprintingDevelopmental BiologyClinical Epigenetics
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New insights into the pathogenesis of Beckwith-Wiedemann and Silver-Russell syndromes: contribution of small copy number variations to 11p15 imprinti…

2011

International audience; The imprinted 11p15 region is organized in two domains, each of them under the control of its own imprinting control region (ICR1 for the IGF2/H19 domain and ICR2 for the KCNQ1OT1/CDKN1C domain). Disruption of 11p15 imprinting results in two fetal growth disorders with opposite phenotypes: the Beckwith-Wiedemann (BWS) and the Silver-Russell (SRS) syndromes. Various 11p15 genetic and epigenetic defects have been demonstrated in BWS and SRS. Among them, isolated DNA methylation defects account for approximately 60% of patients. To investigate whether cryptic copy number variations (CNVs) involving only part of one of the two imprinted domains account for 11p15 isolated…

MaleBeckwith–Wiedemann syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsMESH: Base SequenceMESH: DNA MethylationCopy-number variationImprinting (psychology)[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)GeneticsComparative Genomic Hybridization0303 health sciencesKCNQ1OT1MESH: Polymorphism Single Nucleotide030305 genetics & hereditycopy number variation11p15 regionPedigreegenomic imprintingMESH: Silver-Russell SyndromeDNA methylationBeckwith-Wiedemann syndromeFemaleMESH: DNA Copy Number VariationsMESH: Beckwith-Wiedemann SyndromeAdultDNA Copy Number VariationsMESH: PedigreeBiologyPolymorphism Single Nucleotide03 medical and health sciences[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansEpigenetics030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: HumansBase SequenceChromosomes Human Pair 11MESH: AdultDNA Methylationmedicine.diseaseMESH: MaleMESH: Genomic ImprintingMESH: Comparative Genomic HybridizationUniparental IsodisomySilver-Russell syndromeMESH: Chromosomes Human Pair 11Genomic imprintingMESH: Femalefetal growthfetal growth.
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A genome screen for genes predisposing to bipolar affective disorder detects a new susceptibility locus on 8q

2001

Bipolar affective disorder (BPAD), also known as manic depressive illness, is a severe psychiatric disorder characterized by episodes of mania and depression. It has a lifetime prevalence of approximately 1% in all human populations. In order to identify chromosomal regions containing genes that play a role in determining susceptibility to this psychiatric condition, we have conducted a complete genome screen with 382 markers (average marker spacing of 9.3 cM) in a sample of 75 BPAD families which were recruited through an explicit ascertainment scheme. Pedigrees were of German, Israeli and Italian origin, respectively. Parametric and non-parametric linkage analysis was performed. The highe…

MaleBipolar DisorderGenotypePopulationPedigree chartLocus (genetics)BiologyNuclear FamilyVeinsGenomic ImprintingGenetic linkageLeukocytesGeneticsmedicineHumansGenetic Predisposition to DiseaseGenetic TestingBipolar disordereducationMolecular BiologyGenetics (clinical)Chromosomes Human Pair 14Geneticseducation.field_of_studyAutosomeChromosome MappingDNAGeneral Medicinemedicine.diseasePedigreePhenotypeChromosomes Human Pair 2FemaleLod Scoremedicine.symptomGenomic imprintingManiaChromosomes Human Pair 16Chromosomes Human Pair 8Microsatellite RepeatsHuman Molecular Genetics
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Dppa3 expression is critical for generation of fully reprogrammed iPS cells and maintenance of Dlk1-Dio3 imprinting.

2014

Reprogramming of mouse somatic cells into induced pluripotent stem cells (iPSCs) often generates partially reprogrammed iPSCs (pre-iPSCs), low-grade chimera forming iPSCs (lg-iPSCs) and fully reprogrammed, high-grade chimera production competent iPSCs (hg-iPSCs). Lg-iPSC transcriptome analysis revealed misregulated Dlk1-Dio3 cluster gene expression and subsequently the imprinting defect at the Dlk1-Dio3 locus. Here, we show that germ-cell marker Dppa3 is present only in lg-iPSCs and hg-iPSCs, and that induction with exogenous Dppa3 enhances reprogramming kinetics, generating all hg-iPSCs, similar to vitamin C (Vc). Conversely, Dppa3-null fibroblasts show reprogramming block at pre-iPSCs sta…

MaleChromosomal Proteins Non-HistoneGreen Fluorescent ProteinsInduced Pluripotent Stem CellsMice TransgenicAscorbic AcidIodide PeroxidaseArticleGenomic ImprintingMiceAnimalsCrosses GeneticMice KnockoutGene Expression ProfilingCalcium-Binding ProteinsDNA MethylationFibroblastsMice Inbred C57BLRepressor ProteinsKineticsGerm CellsRetroviridaeGene Expression RegulationIntercellular Signaling Peptides and ProteinsFemaleProtein BindingNature communications
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Comparative methylation profiles and telomerase biology of mouse multipotent adult germline stem cells and embryonic stem cells.

2009

Recently, several groups described the isolation of mouse spermatogonial stem cells (SSCs) and their potential to develop to embryonic stem cell (ESC)-like cells, so-called multipotent germline stem cells (mGSCs). We were the first to derive such mGSCs from SSCs isolated from adult mouse testis and, therefore, called these mGSCs multipotent adult germline stem cells (maGSCs). Here, we compara- tively analyzed gene-specific and global DNA methylation profiles as well as the telomerase biology of several maGSC and male ESC lines. We show that undifferentiated maGSCs are very similar to undifferentiated male ESCs with regard to global DNA methylation, methylation of pluripotency marker gene lo…

MaleEmbryologyAdult Germline Stem CellsTelomeraseSomatic cellBiologyPolymerase Chain ReactionGermline03 medical and health sciencesMice0302 clinical medicineGeneticsAnimalsMolecular BiologyTelomeraseCells CulturedEmbryonic Stem Cells030304 developmental biology0303 health sciencesMultipotent Stem CellsObstetrics and GynecologyCell DifferentiationCell BiologyDNA MethylationMolecular biologyEmbryonic stem cell3. Good healthReproductive Medicine030220 oncology & carcinogenesisDNA methylationElectrophoresis Polyacrylamide GelFemaleStem cellGenomic imprintingDevelopmental BiologyMolecular human reproduction
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The Choice of the Filtering Method in Microarrays Affects the Inference Regarding Dosage Compensation of the Active X-Chromosome

2011

BackgroundThe hypothesis of dosage compensation of genes of the X chromosome, supported by previous microarray studies, was recently challenged by RNA-sequencing data. It was suggested that microarray studies were biased toward an over-estimation of X-linked expression levels as a consequence of the filtering of genes below the detection threshold of microarrays.Methodology/principal findingsTo investigate this hypothesis, we used microarray expression data from circulating monocytes in 1,467 individuals. In total, 25,349 and 1,156 probes were unambiguously assigned to autosomes and the X chromosome, respectively. Globally, there was a clear shift of X-linked expressions toward lower levels…

MaleMicroarrayMicroarraysScienceGene ExpressionBiologyMonocytesGenomic ImprintingMiceX Chromosome InactivationGenes X-LinkedDosage Compensation GeneticMolecular Cell BiologyGeneticsAnimalsHumansRNA MessengerBiologyX-linked recessive inheritanceX chromosomeOligonucleotide Array Sequence AnalysisGeneticsChromosomes Human XMultidisciplinaryDosage compensationAutosomeModels GeneticChromosome BiologyGene Expression ProfilingQRComputational BiologyGenomicsGene expression profilingHEK293 CellsMedicineEpigeneticsFemaleDNA microarrayGenomic imprintingGenome Expression AnalysisResearch ArticlePLoS ONE
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