ArticleNucleic acids research2021
Methylation-directed acetylation of histone H3 regulates developmental sensitivity to histone deacetylase inhibition.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
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- Common oncogenic mutations in colorectal cancer: drivers of carcinogenesis and potential therapeutic targets.Frontiers in pharmacology · 2026Review
- Metabolomics, Genetics, and Environmental Factors: Intersecting Paths in Abdominal Aortic Aneurysm.International journal of molecular sciences · 2025Article
- Unlocking the Epigenetic Symphony: Histone Acetylation Orchestration in Bone Remodeling and Diseases.Stem cell reviews and reports · 2025Review
- mTORC1 pathway activity biases cell fate choice.Scientific reports · 2024Article
- Therapeutic targeting Tudor domains in leukemia via CRISPR-Scan Assisted Drug Discovery.Science advances · 2024Article
- Acetylation-dependent SAGA complex dimerization promotes nucleosome acetylation and gene transcription.Nature structural & molecular biology · 2022Article
- RIOX1-demethylated cGAS regulates ionizing radiation-elicited DNA repair.Bone research · 2022Article
- Histone Lysine Methylation Modification and Its Role in Vascular Calcification.Frontiers in endocrinology · 2022Review
- Moving the Research Forward: The Best of British Biology Using the Tractable Model SystemCells · 2021Review
- The SAGA core module is critical during Drosophila oogenesis and is broadly recruited to promoters.PLoS genetics · 2021Article
- Review
- Histone Methylation Related Therapeutic Challenge in Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hydroxamate-based lysine deacetylase inhibitors (KDACis) are approved for clinical use against certain cancers. However, intrinsic and acquired resistance presents a major problem. Treatment of cells with hydroxamates such as trichostatin A (TSA) leads to rapid preferential acetylation of histone H3 already trimethylated on lysine 4 (H3K4me3), although the importance of this H3K4me3-directed acetylation in the biological consequences of KDACi treatment is not known. We address this utilizing Dictyostelium discoideum strains lacking H3K4me3 due to disruption of the gene encoding the Set1 methyltransferase or mutations in endogenous H3 genes. Loss of H3K4me3 confers resistance to TSA-induced developmental inhibition and delays accumulation of H3K9Ac and H3K14Ac. H3K4me3-directed H3Ac is mediated by Sgf29, a subunit of the SAGA acetyltransferase complex that interacts with H3K4me3 via a tandem tudor domain (TTD). We identify an Sgf29 orthologue in Dictyostelium with a TTD that specifically recognizes the H3K4me3 modification. Disruption of the gene encoding Sgf29 delays accumulation of H3K9Ac and abrogates H3K4me3-directed H3Ac. Either loss or overexpression of Sgf29 confers developmental resistance to TSA. Our results demonstrate that rapid acetylation of H3K4me3 histones regulates developmental sensitivity to TSA. Levels of H3K4me3 or Sgf29 will provide useful biomarkers for sensitivity to this class of chemotherapeutic drug.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.