Publication Details

Category Text Publication
Reference Category Journals
DOI 10.15252/msb.20156520
Title (Primary) Environment-induced epigenetic reprogramming in genomic regulatory elements in smoking mothers and their children
Author Bauer, T.; Trump, S.; Ishaque, N.; Thürmann, L.; Gu, L.; Bauer, M.; Bieg, M.; Gu, Z.; Weichenhan, D.; Mallm, J.-P.; Röder, S. ORCID logo ; Herberth, G. ORCID logo ; Takada, E.; Mücke, O.; Winter, M.; Junge, K.M.; Grützmann, K.; Rolle-Kampczyk, U.; Wang, Q.; Lawerenz, C.; Borte, M.; Polte, T.; Schlesner, M.; Schanne, M.; Wiemann, S.; Geörg, C.; Stunnenberg, H.G.; Plass, C.; Rippe, K.; Mizuguchi, J.; Herrmann, C.; Eils, R.; Lehmann, I.
Source Titel Molecular Systems Biology
Year 2016
Volume 12
Issue 3
Page From art. 861
Language englisch
UFZ wide themes RU3;
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.
Persistent UFZ Identifier
Bauer, T., Trump, S., Ishaque, N., Thürmann, L., Gu, L., Bauer, M., Bieg, M., Gu, Z., Weichenhan, D., Mallm, J.-P., Röder, S., Herberth, G., Takada, E., Mücke, O., Winter, M., Junge, K.M., Grützmann, K., Rolle-Kampczyk, U., Wang, Q., Lawerenz, C., Borte, M., Polte, T., Schlesner, M., Schanne, M., Wiemann, S., Geörg, C., Stunnenberg, H.G., Plass, C., Rippe, K., Mizuguchi, J., Herrmann, C., Eils, R., Lehmann, I. (2016):
Environment-induced epigenetic reprogramming in genomic regulatory elements in smoking mothers and their children
Mol. Syst. Biol. 12 (3), art. 861 10.15252/msb.20156520