Search results for "genomic imprinting"

showing 10 items of 60 documents

ADHD and DAT1: Further evidence of paternal over-transmission of risk alleles and haplotype

2010

Contains fulltext : 87259.pdf (Publisher’s version ) (Closed access) We [Hawi et al. (2005); Am J Hum Genet 77:958-965] reported paternal over-transmission of risk alleles in some ADHD-associated genes. This was particularly clear in the case of the DAT1 3'-UTR VNTR. In the current investigation, we analyzed three new sample comprising of 1,248 ADHD nuclear families to examine the allelic over-transmission of DAT1 in ADHD. The IMAGE sample, the largest of the three-replication samples, provides strong support for a parent of origin effect for allele 6 and the 10 repeat allele (intron 8 and 3'-UTR VNTR, respectively) of DAT1. In addition, a similar pattern of over-transmission of paternal ri…

Untranslated region2716 Genetics (clinical)Candidate gene2804 Cellular and Molecular NeuroscienceMedizin610 Medicine & healthMinisatellite RepeatsBiology2738 Psychiatry and Mental HealthGenomic Imprinting03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineSDG 3 - Good Health and Well-beingmental disordersPerception and Action [DCN 1]HumansGenetics(clinical)ddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersRisk factorAllele3' Untranslated RegionsNuclear familyGeneAllelesGenetics (clinical)GeneticsMental Health [NCEBP 9]Dopamine Plasma Membrane Transport ProteinsHaplotypeIntron10058 Department of Child and Adolescent Psychiatry030227 psychiatryPsychiatry and Mental healthHaplotypesAttention Deficit Disorder with Hyperactivity/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being030217 neurology & neurosurgeryAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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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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Conserved synteny of mammalian imprinted genes in chicken, frog, and fish genomes

2006

Conservation of synteny of mammalian imprinted genes between chicken and human suggested that highly conserved gene clusters were selected long before these genes were recruited for genomic imprinting in mammals. Here we have applied in silico mapping of orthologous genes in pipid frog, zebrafish, spotted green and Japanese pufferfish to show considerable conservation of synteny in lower vertebrates. More than 400 million years ago in a common ancestor of teleost fish and tetrapods, ‘preimprinted’ chromosome regions homologous to human 6q25, 7q21, 7q32, 11p15, and 15q11→q12 already contained most present-day mammalian imprinted genes. Interestingly, some imprinted gene orthologues which are…

GeneticsGenomeBiologySyntenyGenomeChromosomesEvolution MolecularConserved SyntenyMultigene FamilyVertebratesGeneticsAnimalsHumansFish <Actinopterygii>Genomic imprintingMolecular BiologyGeneGenetics (clinical)SyntenyCytogenetic and Genome Research
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Genomic conflicts and sexual antagonism in human health: Insights from oxytocin and testosterone

2015

We review the hypothesized and observed effects of two of the major forms of genomic conflicts, genomic imprinting and sexual antagonism, on human health. We focus on phenotypes mediated by peptide and steroid hormones (especially oxytocin and testosterone) because such hormones centrally mediate patterns of physical and behavioral resource allocation that underlie both forms of conflict. In early development, a suite of imprinted genes modulates the human oxytocinergic system as predicted from theory, with paternally inherited gene expression associated with higher oxytocin production, and increased solicitation to mothers by infants. This system is predicted to impact health through the i…

kinship theoryparental antagonismsexual conflictsexual antagonismparent–offspring conflictgenomic imprinting
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Imprint switching on human chromosome 15 may involve alternative transcripts of the SNRPN gene

1996

Imprinting on human chromosome 15 is regulated by an imprinting centre, which has been mapped to a 100–kb region including exon 1 of SNRPN. From this region we have identified novel transcripts, which represent alternative transcripts of the SNRPN gene. The novel exons lack protein coding potential and are expressed from the paternal chromosome only. We have also identified intragenic deletions and a point mutation in patients who have Angelman or Prader–Willi syndrome due to a parental imprint switch failure. This suggests that imprint switching on human chromosome 15 may involve alternative SNRPN transcripts.

Geneticscongenital hereditary and neonatal diseases and abnormalitiesChromosome 15ExonAlternative splicingHappy puppet syndromeGeneticsBiologyImprinting (psychology)Genomic imprintingGeneSNRPN GeneNature Genetics
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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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Expression profiling of uniparental mouse embryos is inefficient in identifying novel imprinted genes

2006

AbstractImprinted genes are expressed from only one allele in a parent-of-origin-specific manner. We here describe a systematic approach to identify novel imprinted genes using quantification of allele-specific expression by Pyrosequencing, a highly accurate method to detect allele-specific expression differences. Sixty-eight candidate imprinted transcripts mapping to known imprinted chromosomal regions were selected from a recent expression profiling study of uniparental mouse embryos and analyzed. Three novel imprinted transcripts encoding putative non-protein-coding RNAs were identified on the basis of parent-of-origin-specific monoallelic expression in E11.5 (C57BL/6 × Cast/Ei)F1 and in…

DNA ComplementaryTranscription GeneticGenomic imprintingMouseParthenogenesisGene ExpressionGenomicsMice Inbred StrainsUniparental embryoBiologyPolymorphism Single NucleotideChromosomesMicePregnancyDatabases GeneticGeneticsAnimalsRNA MessengerAlleleGeneAllelesCrosses GeneticGeneticsModels GeneticChromosome MappingGenetic VariationPyrosequencingEmbryoParthenogenesisDNAEmbryo MammalianGene expression profilingGene expression profilingMice Inbred C57BLPyrosequencingRNAFemaleGenomic imprintingPrader-Willi SyndromeSoftwareGenomics
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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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Genomic Imprinting and the Regulation of Postnatal Neurogenesis

2017

Most genes required for mammalian development are expressed from both maternally and paternally inherited chromosomal homologues. However, there are a small number of genes known as “imprinted genes” that only express a single allele from one parent, which is repressed on the gene from the other parent. Imprinted genes are dependent on epigenetic mechanisms such as DNA methylation and post-translational modifications of the DNA-associated histone proteins to establish and maintain their parental identity. In the brain, multiple transcripts have been identified which show parental origin-specific expression biases. However, the mechanistic relationship with canonical imprinting is unknown. R…

0301 basic medicineGeneticsReviewBiologyGene dosage03 medical and health sciences030104 developmental biology0302 clinical medicineHistoneDNA methylationbiology.proteinGeneral Earth and Planetary SciencesEpigeneticsImprinting (psychology)AlleleGenomic imprintingGene030217 neurology & neurosurgeryGeneral Environmental ScienceBrain Plasticity
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Extreme Methylation Values of Imprinted Genes in Human Abortions and Stillbirths

2010

Imprinted genes play an important role in fetal and placental development. Using quantitative bisulfite pyrosequencing assays, we determined the DNA methylation levels at two paternally methylated (H19 and MEG3) and four maternally methylated (LIT1, NESP55, PEG3, and SNRPN) imprinted regions in fetal muscle samples from abortions and stillbirths. Two of 55 (4%) spontaneous abortions and 10 of 57 (18%) stillbirths displayed hypermethylation in multiple genes. Interestingly, none of 34 induced abortions had extreme methylation values in multiple genes. All but two abortions/stillbirths with multiple methylation abnormalities were male, indicating that the male embryo may be more susceptible t…

GeneticsRegulation of gene expressionMEG3FetusMusclesShort CommunicationsGene Expression Regulation DevelopmentalAbortion InducedMethylationDNA MethylationStillbirthBiologyfemale genital diseases and pregnancy complicationsPathology and Forensic MedicineGenomic ImprintingFetusPregnancyembryonic structuresDNA methylationHumansFemaleAlleleGenomic imprintingGenereproductive and urinary physiologyThe American Journal of Pathology
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