ArticleGenetics2015
Interplay between histone H3 lysine 56 deacetylation and chromatin modifiers in response to DNA damage.
Article in Genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Chromatin architecture sets origin licensing capacity.Research square · 2026Article
- Chromatin architecture sets origin licensing capacity.bioRxiv : the preprint server for biology · 2026Article
- Persistent Acetylation of Histone H3 Lysine 56 Compromises the Activity of DNA Replication Origins.Molecular and cellular biology · 2023Article
- An epigenetically inherited UV hyper-resistance phenotype in Saccharomyces cerevisiae.Epigenetics & chromatin · 2022Article
- Potential functions of histone H3.3 lysine 56 acetylation in mammals.Epigenetics · 2022Article
- Histone acetylation dynamics in repair of DNA double-strand breaks.Frontiers in genetics · 2022Review
- Chk1 Inhibition Hinders the Restoration of H3.1K56 and H3.3K56 Acetylation and Reprograms Gene Transcription After DNA Damage Repair.Frontiers in oncology · 2022Article
- Effects of sirtuins on the riboflavin production in Ashbya gossypii.Applied microbiology and biotechnology · 2021Article
- Histones on fire: the effect of Dun1 and Mrc1 on origin firing and replication of hyper-acetylated genomes.Current genetics · 2021Review
- Deacetylation of H4 lysine16 affects acetylation of lysine residues in histone H3 and H4 and promotes transcription of constitutive genes.Epigenetics · 2021Article
- Review
- A novel role for Dun1 in the regulation of origin firing upon hyper-acetylation of H3K56.PLoS genetics · 2021Article
- Histone H3 Lysine 56 Acetylation Is Required for Formation of Normal Levels of Meiotic DNA Breaks inFrontiers in cell and developmental biology · 2019Article
- An interplay between multiple sirtuins promotes completion of DNA replication in cells with short telomeres.PLoS genetics · 2018Article
- A Novel Histone Crosstalk Pathway Important for Regulation of UV-Induced DNA Damage Repair inGenetics · 2017Article
- Nicotinamide Suppresses the DNA Damage Sensitivity of Saccharomyces cerevisiae Independently of Sirtuin Deacetylases.Genetics · 2016Article
- Multi-BRCT scaffolds use distinct strategies to support genome maintenance.Cell cycle (Georgetown, Tex.) · 2016Review
- Chromosome-wide histone deacetylation by sirtuins prevents hyperactivation of DNA damage-induced signaling upon replicative stress.Nucleic acids research · 2016Article
- Hst3p, a histone deacetylase, promotes maintenance of Saccharomyces cerevisiae chromosome III lacking efficient replication origins.Molecular genetics and genomics : MGG · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
In Saccharomyces cerevisiae, histone H3 lysine 56 acetylation (H3K56Ac) is present in newly synthesized histones deposited throughout the genome during DNA replication. The sirtuins Hst3 and Hst4 deacetylate H3K56 after S phase, and virtually all histone H3 molecules are K56 acetylated throughout the cell cycle in hst3∆ hst4∆ mutants. Failure to deacetylate H3K56 causes thermosensitivity, spontaneous DNA damage, and sensitivity to replicative stress via molecular mechanisms that remain unclear. Here we demonstrate that unlike wild-type cells, hst3∆ hst4∆ cells are unable to complete genome duplication and accumulate persistent foci containing the homologous recombination protein Rad52 after exposure to genotoxic drugs during S phase. In response to replicative stress, cells lacking Hst3 and Hst4 also displayed intense foci containing the Rfa1 subunit of the single-stranded DNA binding protein complex RPA, as well as persistent activation of DNA damage-induced kinases. To investigate the basis of these phenotypes, we identified histone point mutations that modulate the temperature and genotoxic drug sensitivity of hst3∆ hst4∆ cells. We found that reducing the levels of histone H4 lysine 16 acetylation or H3 lysine 79 methylation partially suppresses these sensitivities and reduces spontaneous and genotoxin-induced activation of the DNA damage-response kinase Rad53 in hst3∆ hst4∆ cells. Our data further suggest that elevated DNA damage-induced signaling significantly contributes to the phenotypes of hst3∆ hst4∆ cells. Overall, these results outline a novel interplay between H3K56Ac, H3K79 methylation, and H4K16 acetylation in the cellular response to DNA damage.
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Registered trials
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.