Histone H4 HDAC activity is necessary for expression of the PU.1 gene
Abstract
Although the current paradigm delegates histone deacetylases (HDACs) to the role of transcriptional co-repressors, we recently showed that HDAC activity was necessary for expression of the hematopoietic transcription factor PU.1. Chromatin immunoprecipitation analyses showed that inhibition of HDACs resulted in increased histone H4 acetylation within the promoter and intron 1 regions of the PU.1 locus. In contrast, increases in both H3 and H4 acetylation were seen for introns 2, 3 and 4 on the 3' end of the PU.1 locus. Maximal increases in histone H4 acetylation over the promoter and intron 1 region were seen within 10 min of HDAC inhibition, while the increases seen on the 3' end showed slower kinetics. The increases in H4 acetylation were reversible and decreased levels of acetylation correlated with re-expression of the PU.1 gene. Finally, we show that HDAC activity is required for association of RNA polymerase II with the PU.1 promoter.
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Inhibition of histone deacetylase increases H4 acetylation and disrupts interaction between the PU.1 locus and RNA polymerase II, suppressing PU.1 transcription in murine microglia.
“Inhibition of histone deacetylase (HDAC) increases acetylation of H4 and disrupts the interaction between the locus and RNA polymerase II, leading to the suppression of PU.1 transcription in murine microglia [35, 36].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [35]
Acetylation of histone H4 on the promoter and intron-1 region of the PU.1 locus is tightly regulated to allow interaction between the locus and RNA polymerase II.
“Acetylation of histone H4 on the promoter and intron-1 region of the PU.1 locus are tightly regulated for allowing the interaction between the locus and RNA polymerase II.”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [35]
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- Authors
- Laribee, R. N., & Klemsz, M. J.
- Affiliations
- Indiana University School of Medicine (US)
- Corresponding author
- Klemsz, Michael J.
- ORCID
- Laribee, R. Nicholas
- Venue
- Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression
- Publisher
- Elsevier BV
- Published
- 2005-09
- Volume
- 1730
- Issue
- 3
- Pages
- 226-234
- ISSN
- 0167-4781 (ISSN-L)
- OpenAlex
- W2083601789
- Cited by
- 11
- References
- 25
- Citations by year
- 2024: 1 · 2023: 2 · 2018: 1 · 2017: 1 · 2016: 1
- FWCI
- 0.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ca071384-05)
- National Cancer Institute (CA-71384)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- histone deacetylase, histone H4 acetylation, hematopoietic transcription factors, corepressors, gene re-expression, hematopoiesis
- MeSH terms
- Proto-Oncogene Protein Spi-1, Acetylation, Animals, Cell Line, Histone Deacetylases, Histones, Hydroxamic Acids, Introns, Kinetics, Promoter Regions, Genetic, Proto-Oncogene Proteins, RNA Polymerase III, Trans-Activators, NIH 3T3 Cells, Cell Line, Tumor, Chromatin Immunoprecipitation, Mice, Histone Deacetylase Inhibitors
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