AP-1 Transcription Factors and the BAF Complex Mediate Signal-Dependent Enhancer Selection
Open accessAbstract
Enhancer elements are genomic regulatory sequences that direct the selective expression of genes so that genetically identical cells can differentiate and acquire the highly specialized forms and functions required to build a functioning animal. To differentiate, cells must select from among the ∼10 6 enhancers encoded in the genome the thousands of enhancers that drive the gene programs that impart their distinct features. We used a genetic approach to identify transcription factors (TFs) required for enhancer selection in fibroblasts. This revealed that the broadly expressed, growth-factor-inducible TFs FOS/JUN (AP-1) play a central role in enhancer selection. FOS/JUN selects enhancers together with cell-type-specific TFs by collaboratively binding to nucleosomal enhancers and recruiting the SWI/SNF (BAF) chromatin remodeling complex to establish accessible chromatin. These experiments demonstrate how environmental signals acting via FOS/JUN and BAF coordinate with cell-type-specific TFs to select enhancer repertoires that enable differentiation during development.
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Many pioneer factors recruit chromatin remodelers.
“The mechanisms of pioneer factor action are still being established [37], but at least some of them (such as FOXA, OCT4 and SOX2/SOX11) have been shown to initiate chromatin opening by direct displacement of histones [38–41], whilst many others recruit chromatin remodelers [42–50].”
From Transcriptional enhancers and their communication with gene promoters (2021) · cites this paper as [50]
The Results section ('AP-1 TFs recruit the BAF complex to enhancers'; page unavailable) supports recruitment of a chromatin remodeler by AP-1. The Discussion describes AP-1 nucleosome binding as a possible pioneer-factor property, but the paper does not establish that many other pioneer factors recruit remodelers. (LLM, conf=0.85)
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- Authors
- Vierbuchen, T., Ling, E., Cowley, C. J., Couch, C. H., Wang, X., Harmin, D. A., Roberts, C. W. M., & Greenberg, M. E.
- Affiliations
- Harvard University (US)
- Dana-Farber Cancer Institute (US)
- St. Jude Children's Research Hospital (US)
- Corresponding author
- Vierbuchen, Thomas
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2017-12
- Volume
- 68
- Issue
- 6
- Pages
- 1067-1082.e12
- ISSN
- 1097-2765 (ISSN-L)
- PMC
- PMC5744881
- OpenAlex
- W2779662045
- Cited by
- 455
- References
- 11
- Citations by year
- 2026: 46 · 2025: 68 · 2024: 53 · 2023: 58 · 2022: 76 · 2021: 40 · 2020: 47 · 2019: 46 · 2018: 20 · 2017: 1
- FWCI
- 12.74
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 385 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (4R37NS028829-28)
- Damon Runyon Cancer Research Foundation (DRG-2177-14)
- National Science Foundation Graduate Research Fellowship (DGE0946799, DGE1144152)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- AP-1 transcription factor, Fos/Jun, BAF chromatin remodeling complex, SWI/SNF complex, cell type-specific transcription factors, chromatin accessibility, cell differentiation, fibroblasts, growth factor signaling
- MeSH terms
- Animals, Chromatin, Chromosomal Proteins, Non-Histone, Enhancer Elements, Genetic, Female, Male, Mice, Inbred C57BL, Nucleosomes, Promoter Regions, Genetic, Transcription Factors, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-fos, Mice, Knockout
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