Search results for "genomic imprinting"

showing 10 items of 60 documents

261 INFLUENCE OF IN VITRO MATURATION ON EPIGENETIC MARKS AND GENE EXPRESSION IN BOVINE OOCYTES

2011

In cattle, in vitro maturation (IVM) of oocytes is an integral part of assisted reproduction technology. However, only 30% of in vitro matured bovine oocytes develop to the blastocyst stage after fertilization (compared with 60% for in vivo matured oocytes), indicating critical involvement of maturation conditions in the developmental competence of oocytes. Oocytes for IVF and intracytoplasmic sperm injection in humans are typically allowed to mature in vivo after superovulation because IVM is not considered to be a safe medical procedure. Several studies have shown that assisted reproduction technology involving prolonged in vitro culture of human and ruminant embryos can be associated wi…

GeneticsReproductive technologyBiologyOocyteOogenesisIn vitro maturationAndrologyEndocrinologyDifferentially methylated regionsmedicine.anatomical_structureReproductive Medicineembryonic structuresDNA methylationGeneticsmedicineAnimal Science and ZoologyEpigeneticsGenomic imprintingMolecular BiologyDevelopmental BiologyBiotechnologyReproduction, Fertility and Development
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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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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…

Geneticskinship theoryReviews and SynthesisBiologygenomic imprintingSexual dimorphismSexual conflictparental antagonismsexual conflictsexual antagonismGeneticsta1181EpigeneticsAlleleParent–offspring conflictGeneral Agricultural and Biological SciencesEvolutionary dynamicsGenomic imprintingEcology Evolution Behavior and Systematicsparent–offspring conflictMaladaptationEvolutionary Applications
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Genomic imprinting and neurodevelopment

2021

Abstract During mammalian development, most genes are equally expressed from both the maternal and the paternal alleles. However, a minority of genes known as “imprinted genes’” are expressed or silenced from either the maternal or the paternal homologue, resulting functionally monoallelic. This process known as “genomic imprinting” is essential for normal development and shows tissue and developmental-stage specificity, suggesting a key role in gene dosage fine-tuning. Furthermore, genomic imprinting is highly prevalent in the brain, and many genes with a key role in pre- and postnatal neurodevelopment are expressed in a parent-of-origin specific manner in the central nervous system. This …

Geneticsmedicine.anatomical_structureCentral nervous systemmedicineBiologyAlleleGenomic imprintingGeneImprinting (organizational theory)Gene dosage
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Ovulation induction and epigenetic anomalies

2013

In this systematic review of ovulation induction and epigenetic control, studies mainly done in the mouse model highlight how hormone treatments may be prejudicial to the epigenetic reprogramming of gametes as well as early embryos. Moreover, the hormone protocols used in assisted reproduction may also modify the physiologic environment of the uterus, a potential link to endometrial epigenetic disturbances. At present, the few available data in humans are insufficient to allow us to independently determine the impact of a woman's age and infertility problems and treatment protocols and hormone doses on such processes as genomic imprinting.

Infertilitymedicine.medical_specialtyReproductive Techniques Assistedmedicine.medical_treatmentBiologyBioinformaticsEpigenesis GeneticMiceOvulation InductionInternal medicinemedicineAnimalsHumansEpigeneticsEpigenesisGenetic Diseases InbornObstetrics and Gynecologymedicine.diseaseEndocrinologyReproductive MedicineModels AnimalDNA methylationFemaleOvulation inductionGenomic imprintingReprogrammingHormoneFertility and Sterility
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Abnormal Hypermethylation at Imprinting Control Regions in Patients with S-Adenosylhomocysteine Hydrolase (AHCY) Deficiency

2016

S-adenosylhomocysteine hydrolase (AHCY) deficiency is a rare autosomal recessive disorder in methionine metabolism caused by mutations in the AHCY gene. Main characteristics are psychomotor delay including delayed myelination and myopathy (hypotonia, absent tendon reflexes etc.) from birth, mostly associated with hypermethioninaemia, elevated serum creatine kinase levels and increased genome wide DNA methylation. The prime function of AHCY is to hydrolyse and efficiently remove S-adenosylhomocysteine, the by-product of transmethylation reactions and one of the most potent methyltransferase inhibitors. In this study, we set out to more specifically characterize DNA methylation changes in blo…

Male0301 basic medicineMethyltransferaselcsh:MedicineArtificial Gene Amplification and ExtensionGlycine N-MethyltransferaseBiochemistryPolymerase Chain Reactionlaw.inventionMethionine0302 clinical medicinelawAmino Acidslcsh:SciencePolymerase chain reactionGeneticsDNA methylationMammalian GenomicsMultidisciplinaryOrganic CompoundsGenomicsMethylationChromatinEnzymes3. Good healthNucleic acidsChemistryPhysical SciencesDNA methylationEpigeneticsFemaleDNA modificationChromatin modificationResearch ArticleChromosome biologyCell biologyAlu elementBiologyResearch and Analysis MethodsGenomic Imprinting03 medical and health sciencesAlu ElementsGeneticsSulfur Containing Amino AcidsHumansRepeated SequencesMolecular Biology TechniquesMolecular BiologyAmino Acid Metabolism Inborn ErrorsGeneBiology and life sciencesOrganic Chemistrylcsh:RChemical CompoundsInfant NewbornProteinsInfantDNAMethyltransferasesCreatineMolecular biologyLong Interspersed Nucleotide Elements030104 developmental biologyDifferentially methylated regionsAnimal GenomicsEnzymologyAHCY ; Hypermethylationlcsh:QGene expressionGenomic imprinting030217 neurology & neurosurgeryDevelopmental BiologyPLOS ONE
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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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