The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Enhancer transcripts mark active estrogen receptor binding sites
Open accessAbstract
We have integrated and analyzed a large number of data sets from a variety of genomic assays using a novel computational pipeline to provide a global view of estrogen receptor 1 (ESR1; a.k.a. ERα) enhancers in MCF-7 human breast cancer cells. Using this approach, we have defined a class of primary transcripts (eRNAs) that are transcribed uni- or bidirectionally from estrogen receptor binding sites (ERBSs) with an average transcription unit length of ∼3–5 kb. The majority are up-regulated by short treatments with estradiol (i.e., 10, 25, or 40 min) with kinetics that precede or match the induction of the target genes. The production of eRNAs at ERBSs is strongly correlated with the enrichment of a number of genomic features that are associated with enhancers (e.g., H3K4me1, H3K27ac, EP300/CREBBP, RNA polymerase II, open chromatin architecture), as well as enhancer looping to target gene promoters. In the absence of eRNA production, strong enrichment of these features is not observed, even though ESR1 binding is evident. We find that flavopiridol, a CDK9 inhibitor that blocks transcription elongation, inhibits eRNA production but does not affect other molecular indicators of enhancer activity, suggesting that eRNA production occurs after the assembly of active enhancers. Finally, we show that an enhancer transcription “signature” based on GRO-seq data can be used for de novo enhancer prediction across cell types. Together, our studies shed new light on the activity of ESR1 at its enhancer sites and provide new insights about enhancer function.
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Cites
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Widespread transcription at neuronal activity-regulated enhancers
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A unique chromatin signature uncovers early developmental enhancers in humans
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Mediator and cohesin connect gene expression and chromatin architecture
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Long Noncoding RNAs with Enhancer-like Function in Human Cells
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“Differential association of these features with enhancers in a given cell may define distinct classes of enhancers that specify distinct gene regulatory mechanisms and biological outcomes (Creyghton et al. 2010; Ghisletti et al. 2010; Rada-Iglesias et al. 2011; Wang et al. 2011; Zentner et al. 2011; Pham et al. 2012;…”
BackgroundA Large Fraction of Extragenic RNA Pol II Transcription Sites Overlap Enhancers
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Cited by
The Mediator complex: a central integrator of transcription
Allen, B. L., & Taatjes, D. J. (2015) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3951 · Cited by 922
Enhancers as non-coding RNA transcription units: recent insights and future perspectives
Li, W., Notani, D., & Rosenfeld, M. G. (2016) · Nature Reviews Genetics · doi:10.1038/nrg.2016.4 · Cited by 710
Core, L. J., Martins, A. L., Danko, C. G., Waters, C. T., Siepel, A., & Lis, J. T. (2014) · Nature Genetics · doi:10.1038/ng.3142 · Cited by 693
Self-citationTranscribed enhancers lead waves of coordinated transcription in transitioning mammalian cells
Arner, E., Daub, C. O., Vitting-Seerup, K., Andersson, R., Lilje, B., Drabløs, F., Lennartsson, A., Rönnerblad, M., Hrydziuszko, O., Vitezic, M., et al. (2015) · Science · doi:10.1126/science.1259418 · Cited by 579
Mahat, D. B., Kwak, H., Booth, G. T., Jonkers, I. H., Danko, C. G., Patel, R. K., Waters, C. T., Munson, K., Core, L. J., & Lis, J. T. (2016) · Nature Protocols · doi:10.1038/nprot.2016.086 · Cited by 508
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Metadata
- Authors
- Hah, N., Murakami, S., Nagari, A., Danko, C. G., & Kraus, W. L.
- Venue
- Genome Research
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2013-05-01
- Volume
- 23
- Issue
- 8
- Pages
- 1210-1223
- ISSN
- 1088-9051 (ISSN-L)
- OpenAlex
- W2152144700
- Cited by
- 476
- References
- 17
- Type
- posted content
- Language
- en
- Open access
- hybrid
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