Histone H3K27ac separates active from poised enhancers and predicts developmental state
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Boyer_Histone H3K27.pdf
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Author(s)
Creyghton, Menno P.
Cheng, Albert W.
Welstead, G. Grant
Kooistra, Tristan G.
Carey, Bryce W.
Steine, Eveline J.
Hanna, Jacob
Lodato, Michael Anthony
Frampton, Garrett M.
Sharp, Phillip A.
Date Issued
November 2010
Journal
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences (U.S.)
Citation
Creyghton, M. P., A. W. Cheng, G. G. Welstead, T. Kooistra, B. W. Carey, E. J. Steine, J. Hanna, et al. “Histone H3K27ac separates active from poised enhancers and predicts developmental state.” Proceedings of the National Academy of Sciences 107, no. 50 (December 14, 2010): 21931-21936.
Version
Final published version
Abstract
Developmental programs are controlled by transcription factors and chromatin regulators, which maintain specific gene expression programs through epigenetic modification of the genome. These regulatory events at enhancers contribute to the specific gene expression programs that determine cell state and the potential for differentiation into new cell types. Although enhancer elements are known to be associated with certain histone modifications and transcription factors, the relationship of these modifications to gene expression and developmental state has not been clearly defined. Here we interrogate the epigenetic landscape of enhancer elements in embryonic stem cells and several adult tissues in the mouse. We find that histone H3K27ac distinguishes active enhancers from inactive/poised enhancer elements containing H3K4me1 alone. This indicates that the amount of actively used enhancers is lower than previously anticipated. Furthermore, poised enhancer networks provide clues to unrealized developmental programs. Finally, we show that enhancers are reset during nuclear reprogramming.
MIT Department
Harvard University--MIT Division of Health Sciences and Technology
Massachusetts Institute of Technology. Computational and Systems Biology Program
Whitehead Institute for Biomedical Research
Koch Institute for Integrative Cancer Research at MIT
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DOI of Published Version
https://doi.org/10.1073/pnas.1016071107
