<HashMap><database>EGA</database><scores/><additional><omics_type>Genomics</omics_type><technology_type>Illumina HiSeq 2000</technology_type><study_type>Epigenetics</study_type><full_dataset_link>https://ega-archive.org/studies/EGAS00001000455</full_dataset_link><host>EGA</host><description>EGA study EGAS00001000455</description><dataset_title>ChIPseq data of child-mother pairs, maternal smoking.</dataset_title><dataset_title>RNA sequencing data of child-mother pairs, maternal smoking.</dataset_title><dataset_title>Whole genome bisufite sequencing for smoking and non-smoking mother-child pairs</dataset_title><category>restricted</category><repository>EGA</repository><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_abstract><pubmed_title>Environment-induced epigenetic reprogramming in genomic regulatory elements in smoking mothers and their children.</pubmed_title><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</pubmed_authors></additional><is_claimable>false</is_claimable><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.</name><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.
RNA-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.

Longitudinal data spanning several years provides the means to investigate the stability of observed differences of all data types.</description><dates><updated>2017-07-26 15:39:27</updated></dates><accession>EGAS00001000455</accession><cross_references><TAXONOMY>9606</TAXONOMY><pubmed>27013061</pubmed><EGA>EGAD00001002012</EGA><EGA>EGAD00001002011</EGA><EGA>EGAD00001000366</EGA><EGA>EGAC00001000452</EGA></cross_references></HashMap>