Transcription Factor AP1 Potentiates Chromatin Accessibility and Glucocorticoid Receptor Binding
Open accessAbstract
Ligand-dependent transcription by the nuclear receptor glucocorticoid receptor (GR) is mediated by interactions with coregulators. The role of these interactions in determining selective binding of GR to regulatory elements remains unclear. Recent findings indicate that a large fraction of genomic GR binding coincides with chromatin that is accessible prior to hormone treatment, suggesting that receptor binding is dictated by proteins that maintain chromatin in an open state. Combining DNaseI accessibility and chromatin immunoprecipitation with high-throughput sequencing, we identify the activator protein 1 (AP1) as a major partner for productive GR-chromatin interactions. AP1 is critical for GR-regulated transcription and recruitment to co-occupied regulatory elements, illustrating an extensive AP1-GR interaction network. Importantly, the maintenance of baseline chromatin accessibility facilitates GR recruitment and is dependent on AP1 binding. We propose a model in which the basal occupancy of transcription factors acts to prime chromatin and direct inducible transcription factors to select regions in the genome.
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Assisted loading has been described in various systems.
“Assisted loading has been described in various systems30–37.”
From Synergistic gene expression during the acute phase response is characterized by transcription factor assisted loading (2017) · cites this paper as [30]
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- Authors
- Biddie, S. C., John, S., Sabo, P. J., Thurman, R. E., Johnson, T. A., Schiltz, R. L., Miranda, T. B., Sung, M.-H., Trump, S., Lightman, S. L., Vinson, C., Stamatoyannopoulos, J. A., & Hager, G. L.
- Affiliations
- National Institutes of Health (US)
- University of Washington (US)
- Helmholtz Centre for Environmental Research (DE)
- University of Bristol (GB)
- Corresponding author
- John, Sam
- Stamatoyannopoulos, John A.
- Hager, Gordon L.
- ORCID
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2011-07
- Volume
- 43
- Issue
- 1
- Pages
- 145-155
- ISSN
- 1097-2765 (ISSN-L)
- PMC
- PMC3138120
- OpenAlex
- W1999319214
- Cited by
- 503
- References
- 3
- Citations by year
- 2026: 27 · 2025: 26 · 2024: 31 · 2023: 18 · 2022: 34 · 2021: 31 · 2020: 29 · 2019: 34 · 2018: 39 · 2017: 33 · 2016: 46 · 2015: 29 · 2014: 32 · 2013: 50 · 2012: 37
- FWCI
- 16.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- Funders
- National Institutes of Health
- National Human Genome Research Institute (RC2HG005654)
- National Cancer Institute (Z01BC010308, Z01BC005450)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- activator protein-1, glucocorticoid receptor, chromatin accessibility, transcription factor binding, coregulators, ligand-dependent transcription, DNase I footprinting, transcriptional regulation
- MeSH terms
- Animals, Binding Sites, Cell Line, Chromatin, Gene Expression Regulation, Ligands, Models, Genetic, Receptors, Glucocorticoid, Genome, Transcription Factor AP-1, Regulatory Elements, Transcriptional, Mice
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