ChIP-seq analysis reveals distinct H3K27me3 profiles that correlate with transcriptional activity
- Author(s)
- Young, MD; Willson, TA; Wakefield, MJ; Trounson, E; Hilton, DJ; Blewitt, ME; Oshlack, A; Majewski, IJ;
- Details
- Publication Year 2011-09,Volume 39,Issue #17,Page 7415-7427
- Journal Title
- NUCLEIC ACIDS RESEARCH
- Publication Type
- Journal Article
- Abstract
- Transcriptional control is dependent on a vast network of epigenetic modifications. One epigenetic mark of particular interest is tri-methylation of lysine 27 on histone H3 (H3K27me3), which is catalysed and maintained by Polycomb Repressive Complex 2 (PRC2). Although this histone mark is studied widely, the precise relationship between its local pattern of enrichment and regulation of gene expression is currently unclear. We have used ChIP-seq to generate genome-wide maps of H3K27me3 enrichment, and have identified three enrichment profiles with distinct regulatory consequences. First, a broad domain of H3K27me3 enrichment across the body of genes corresponds to the canonical view of H3K27me3 as inhibitory to transcription. Second, a peak of enrichment around the transcription start site (TSS) is commonly associated with 'bivalent' genes, where H3K4me3 also marks the TSS. Finally and most surprisingly, we identified an enrichment profile with a peak in the promoter of genes that is associated with active transcription. Genes with each of these three profiles were found in different proportions in each of the cell types studied. The data analysis techniques developed here will be useful for the identification of common enrichment profiles for other histone modifications that have important consequences for transcriptional regulation.
- Publisher
- OXFORD UNIV PRESS
- Keywords
- EMBRYONIC STEM-CELLS; DEVELOPMENTAL REGULATORS; CHROMATIN SIGNATURES; HUMAN GENOME; POLYCOMB; GENES; PLURIPOTENT; DIFFERENTIATION; COMMITMENT; MECHANISMS
- Research Division(s)
- Molecular Medicine; Bioinformatics
- Publisher's Version
- https://doi.org/10.1093/nar/gkr416
- Open Access at Publisher's Site
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177187/- Terms of Use/Rights Notice
- Copyright © The Author(s) 2011. Published by Oxford University Press.
Creation Date: 2011-09-01 12:00:00