{"database":"EGA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics","Multiomics"],"technology_type":["Illumina HiSeq 2000"],"study_type":["Epigenetics"],"full_dataset_link":["https://ega-archive.org/studies/EGAS00001000455"],"host":["EGA"],"description":["EGA study EGAS00001000455"],"dataset_title":["ChIPseq data of child-mother pairs, maternal smoking.","RNA sequencing data of child-mother pairs, maternal smoking.","Whole genome bisufite sequencing for smoking and non-smoking mother-child pairs"],"category":["restricted"],"repository":["EGA"],"pubmed_abstract":["Epigenetic mechanisms have emerged as links between prenatal environmental exposure and disease risk later in life. Here, we studied epigenetic changes associated with maternal smoking at base pair resolution by mapping DNA methylation, histone modifications, and transcription in expectant mothers and their newborn children. We found extensive global differential methylation and carefully evaluated these changes to separate environment associated from genotype-related DNA methylation changes. Differential methylation is enriched in enhancer elements and targets in particular \"commuting\" enhancers having multiple, regulatory interactions with distal genes. Longitudinal whole-genome bisulfite sequencing revealed that DNA methylation changes associated with maternal smoking persist over years of life. Particularly in children prenatal environmental exposure leads to chromatin transitions into a hyperactive state. Combined DNA methylation, histone modification, and gene expression analyses indicate that differential methylation in enhancer regions is more often functionally translated than methylation changes in promoters or non-regulatory elements. Finally, we show that epigenetic deregulation of a commuting enhancer targeting c-Jun N-terminal kinase 2 (JNK2) is linked to impaired lung function in early childhood."],"pubmed_title":["Environment-induced epigenetic reprogramming in genomic regulatory elements in smoking mothers and their children."],"pubmed_authors":["Bauer Tobias T, Trump Saskia S, Ishaque Naveed N, Thürmann Loreen L, Gu Lei L, Bauer Mario M, Bieg Matthias M, Gu Zuguang Z, Weichenhan Dieter D, Mallm Jan-Philipp JP, Röder Stefan S, Herberth Gunda G, Takada Eiko E, Mücke Oliver O, Winter Marcus M, Junge Kristin M KM, Grützmann Konrad K, Rolle-Kampczyk Ulrike U, Wang Qi Q, Lawerenz Christian C, Borte Michael M, Polte Tobias T, Schlesner Matthias M, Schanne Michaela M, Wiemann Stefan S, Geörg Christina C, Stunnenberg Hendrik G HG, Plass Christoph C, Rippe Karsten K, Mizuguchi Junichiro J, Herrmann Carl C, Eils Roland R, Lehmann Irina I"],"name_synonyms":["HITS-CLIP, High Throughput Sequencing of RNA Isolated by Crosslinking Immunoprecipitation, ChIP-Chip, cHILD, young adult, pediatric interstitial lung disease, Chromatin Immuno-precipitation, whole blood, Smoking Behavior, Blood, Cross Linking and Immunoprecipitation Followed by Deep Sequencing, follow up., ChIP Sequencing, RNA-seq, Parturitions, CLIP-Seq, Assay for Transposase-Accessible Chromatin Using Sequencing, Behavior, ChIP-PET, ChIP-Exo, Pregnancies, PREGN, Births, CHILD, PBMC, Smoking Habit, Chromatin Immunoprecipitation Sequencing-Chip, Whole Transcriptome Shotgun Sequencing, High-Throughput Sequencing of RNA Isolated by Crosslinking Immunoprecipitation, interstitial lung disease of childhood, ChIA-PET, Smoking, child, Chromatin Immunoprecipitation Sequencing Chip, tobacco use disorder, Chromatin Immuno precipitation Sequencing, carrying of young, Peripheral Blood, ILD specific to childhood, Gestation, ChIP, Birth, Chromatin Immunoprecipitation Paired End Tag, Chromatin Immuno Precipitation Paired End Tag, Cross-Linking and Immunoprecipitation Followed by Deep Sequencing, chILD syndrome, Chromatin Immunoprecipitation, Mother, Chromatin Immuno-precipitation Sequencing, whole genome, smoking, ChIP Exonuclease, Children, ChIP-Seq, paediatric interstitial lung disease, Sequencing, Assay for Transposase Accessible Chromatin Using Sequencing, chILD, Chromatin Immunoprecipitation Paired-End Tag, Reticuloendothelial System, juvenile stage, Smoking Habits, children's interstitial lung disease, childhood interstitial lung disease, Chromatin Immuno-Precipitation Paired-End Tag, PBMCs, Smoking Behaviors, ATAC-Seq, Chromatin Immunoprecipitation Sequencing-Chips, Habit, Behaviors, Childbirths, ChIP-Exonuclease, Habits, Childbirth"],"description_synonyms":["HSPABP2, H2S(D2S), Ribonucleic, cytoplasmic chromatin, young adult, region or site annotation, Smoking Behavior, 2210017D18Rik, dCHIP, Gene, SCAR16, Ximpact, DmelCG5203, CHILD, Gene Products, interstitial lung disease of childhood, Non Polyadenylated, 2310040B03Rik, Chromatins, RNA Gene Products, imprinted and ancient gene protein, study, positional, NY-CO-7, Gene Expressions, Chip, ChIP, CHIP, bisulfite, Expressions, paediatric interstitial lung disease, Epigenomic, chILD, Non-Polyadenylated RNA, juvenile stage, chip, geographical area, Smoking Habits, childhood interstitial lung disease, DmelCG3924, chromosome scaffold, Habit, AW046544, Expression, UBOX1, associated, Behaviors, 0610033N24Rik, PP1131, single-organism behavior, nuclear chromatin, Gene., RNA, l(2)k04405, cHILD, whole blood, pediatric interstitial lung disease, Data Set, hydrosulfite, ribose nucleic acid, ribonucleic acids, CG5203, RNS, l(2)04405, Behavior, impact-a, yeast nucleic acid, Ribonukleinsaeure, Smoking Habit, sequence, pentosenucleic acids, imprinted and ancient gene protein homolog, IMPACT, Ribonucleic acids, SDCCAG7, child, Smoking, ribonucleic acid, Acid, tobacco use disorder, dLdb, positional polypeptide feature, ILD specific to childhood, Ldb, LDB, Epigenetic, Non Polyadenylated RNA, Non-Polyadenylated, chILD syndrome, Chromatin Immunoprecipitation, smoking, Ribonucleic Acid, CG3924, Children, primary structure of sequence macromolecule, dLDB/Chip, children's interstitial lung disease, Smoking Behaviors, Epigenetics, E430016J11Rik, RWDD5, Habits"],"pubmed_title_synonyms":["tobacco use disorder, Element, Epigenetic, Smoking Behavior, atoms, Mother, smoking, Behavior, Epigenomic, element, Impact, Environmental Impact, Environmental, Smoking Habits, Smoking Behaviors, Smoking Habit, Environments, Habit, Impacts, atomo, atomus, Environmental Impacts, elements, Epigenetics, Behaviors, atome, atom, Children., Habits, Smoking"],"pubmed_abstract_synonyms":["Kinase-2, Neonates, H2S(D2S), Enhancer, Mitogen Activated Protein Kinase 9, Materials, Commuting, 2.7.11.24, SAPK-alpha, JNK-55, Neonate, c-Jun N-terminal kinase 2, DNA Methylations, Genetic Enhancer Element, element, JNK2B, JNK2A, Relative, Transcript Expression Analysis, diseases, Exposure, parenchyma of lung, Code, Gene Expression Monitorings, Stress Activated Protein Kinase JNK2, Impacts, diseases and disorders, Analysis, Profilings, Environmental Impacts, Fs(3)Hor, Chromatins, Histone Mark, human disease, DmelCG2684, DNA methylation maintenance, c-jun N-terminal Kinase 2, Stress-Activated Protein Kinase JNK2, Genomes, Analyses, Elements, entire life cycle, Genetic Enhancer, DNA methylation, NTef2, Epigenomic, MAPK9 Mitogen Activated Protein Kinase, Environmental Impact, Gene Expression Analysis, c-jun Kinase-2, chromosome scaffold, JNK2ALPHA, Homo sapiens disease, transcription from bacterial-type RNA polymerase promoter, Base Pairings, Newborn Infants, nuclear chromatin, NEWBORN (0-27 DAYS), Exposures, pulmo, Modifications, Monitorings, lung parenchyma, p54aSAPK, Gene Expression, Histone Modifications, Relative Risks, Diseases, Newborn Infant, Enhancer Element, Genetic Materials, atomo, JNK2 Stress Activated Protein Kinase, Enhancer Sequence, atome, JNK2 Kinase, Genetic Material, neoplasms, Smoking, Stress-activated protein kinase JNK2, tobacco use disorder, Element, Risk, Mark, Epigenetic, Transcriptome Profilings, life, atoms, Newborns, whole genome, Children, MAPK9 Mitogen-Activated Protein Kinase, early, disease, Gene Expression Analyses, Histone Marks, pulmonary, Material, Horka, bacterial transcription, SAPK, CG2684, Fs(3)Horka, Cistron, Expression Analysis, DNA, Fs(3)Sz11., Epigenetics, Methylation, p54a, other disease, cytoplasmic chromatin, lifespan, Smoking Behavior, Gene, Gene Expression Profilings, mRNA Differential Displays, Gene Expression Pattern Analysis, Prkm9, lung, disease or disorder, JNK2 Stress-Activated Protein Kinase, DmF2, Environmental Exposures, c jun N terminal Kinase 2, neoplasm, lod, Genetic, entire lifespan, Marks, c jun Kinase 2, Mother, bisulfite, Transcriptomics, Transcript Expression, Transcriptome Analysis, PRKM9, Genotypes, Monitoring, non-neoplastic, Enhancer Elements, Smoking Habits, Base Pair, Habit, disorder, elements, Behaviors, Expression Analyses, Methylations, atom, Neonatal, SAPK1a, Profiling, p54-alpha, Transcriptome, Infants, hydrosulfite, c-jun, disorders, medical condition, function, Behavior, Cistrons, AI851083, Histone, Impact, Environmental, Sequences, Differential Display, Transcript Expression Analyses, Stress-activated protein kinase 1a, Genogroup, JNK2, Sequence, Smoking Habit, MAP kinase 9, condition, Genetic Enhancer Elements, atomus, methylation, mRNA Differential Display, INSDC_feature:regulatory, Relative Risk, Base Pairs, Gene Expression Monitoring, histone modification site, Transcriptome Profiling, mRNA, Risks, smoking, Differential Displays, Lds, Transcriptome Analyses, Genogroups, JNK2BETA, Smoking Behaviors, Enhancer Sequences, Environments, Newborn, Lungs, MAPK 9, Habits"],"additional_accession":[]},"is_claimable":false,"name":"Whole genome bisufite sequencing of smoking and non-smoking mother-child pairsBisufite sequencing, RNA-seq and ChIP-Seq data of whole blood samples from smoking and non-smoking mothers and their children at gestation/birth and follow-up years.","description":"Whole-blood samples of 16 mother-child pairs with differing maternal smoking behaviour were bisulfite treated and sequenced with deep coverage to identify smoking-associated differentially methylated regions.\nRNA-sequencing and ChIP-sequencing of 4 chromatin marks complete the data set and allow for integrative analyses, functional region annotation and to study the impact of epigenetic changes on gene expression.\n\nLongitudinal data spanning several years provides the means to investigate the stability of observed differences of all data types.","dates":{"updated":"2017-07-26 15:39:27"},"accession":"EGAS00001000455","cross_references":{"TAXONOMY":["9606"],"pubmed":["27013061"],"EGA":["EGAD00001002012","EGAD00001002011","EGAD00001000366","EGAC00001000452"]}}