ArticleThe Journal of biological chemistry2016
Chromatin Remodeler Recruitment during Macrophage Differentiation Facilitates Transcription Factor Binding to Enhancers in Mature Cells.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Therapeutic targeting SPI1 in combination with erastin promotes ferroptosis in ccRCC.Communications biology · 2025Article
- Regulatory Roles of SWI/SNF Chromatin Remodeling Complexes in Immune Response and Inflammatory Diseases.Clinical reviews in allergy & immunology · 2024Review
- A complex network of transcription factors and epigenetic regulators involved in bovine leukemia virus transcriptional regulation.Retrovirology · 2023Review
- SWI/SNF chromatin remodelers in prostate cancer progression.Frontiers in epigenetics and epigenomics · 2023Review
- HDAC1 and PRC2 mediate combinatorial control in SPI1/PU.1-dependent gene repression in murine erythroleukaemia.Nucleic acids research · 2022Article
- One genome, many cell states: epigenetic control of innate immunity.Current opinion in immunology · 2022Review
- The autophagy protein Ambra1 regulates gene expression by supporting novel transcriptional complexes.The Journal of biological chemistry · 2020Article
- Control of Stimulus-Dependent Responses in Macrophages by SWI/SNF Chromatin Remodeling Complexes.Trends in immunology · 2020Review
- EWS-FLI1 modulated alternative splicing of ARID1A reveals novel oncogenic function through the BAF complex.Nucleic acids research · 2019Article
- Pioneering, chromatin remodeling, and epigenetic constraint in early T-cell gene regulation by SPI1 (PU.1).Genome research · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We show how enhancers of macrophage-specific genes are rendered accessible in differentiating macrophages to allow their induction in mature cells in response to an appropriate stimulus. Using a lentiviral knockdown approach in primary differentiating macrophages from mouse bone marrow, we demonstrate that enhancers of Il12b and Il1a are kept relatively lowly occupied by nucleosomes and accessible through recruitment of the nucleosome remodeler BAF/PBAF. Our results using an inducible cell line that expresses an estrogen receptor fusion of the macrophage-specific transcription factor PU.1 (PUER) show that BAF/PBAF recruitment to these enhancers is a consequence of translocation of PUER to the nucleus in the presence of tamoxifen, and we speculate that remodeler recruitment may be directly mediated by PU.1. In the absence of BAF/PBAF recruitment, nucleosome occupancy at the enhancer of Il12b (and to a lesser extent at Il1a) reaches high levels in bone marrow-derived macrophages (BMDMs), and the enhancers are not fully cleared of nucleosomes upon LPS induction, resulting in impaired gene expression. Analysis of Il12b expression in single cells suggests that recruitment of the remodeler is necessary for high levels of transcription from the same promoter, and we propose that remodelers function by increasing nucleosome turnover to facilitate transcription factor over nucleosome binding in a process we have termed "remodeler-assisted competition."
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