ArticlePLoS genetics2013
A reversible histone H3 acetylation cooperates with mismatch repair and replicative polymerases in maintaining genome stability.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Two sirtuin proteins, Hst3 and Hst4, modulate asexual development, stress tolerance, and virulence by affecting global gene expression inMicrobiology spectrum · 2024Article
- Genetic inhibitors of APOBEC3B-induced mutagenesis.Genome research · 2023Article
- Chromatin structure influences rate and spectrum of spontaneous mutations inGenome research · 2023Article
- [PRIONPathogens (Basel, Switzerland) · 2022Article
- Incorporation of a histone mutant with H3K56 site substitution perturbs the replication machinery in mouse embryonic stem cells.Journal of molecular cell biology · 2022Article
- The nuclease activity of DNA2 promotes exonuclease 1-independent mismatch repair.The Journal of biological chemistry · 2022Article
- Review
- Review
- Gene repression in S. cerevisiae-looking beyond Sir-dependent gene silencing.Current genetics · 2021Review
- Chromatin Structure and Drug Resistance inJournal of fungi (Basel, Switzerland) · 2020Review
- Article
- Mutational signatures of redox stress in yeast single-strand DNA and of aging in human mitochondrial DNA share a common feature.PLoS biology · 2019Article
- Involvement of DNA mismatch repair in the maintenance of heterochromatic DNA stability in Saccharomyces cerevisiae.PLoS genetics · 2017Article
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
- Interaction of proliferating cell nuclear antigen with PMS2 is required for MutLα activation and function in mismatch repair.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Yeast DNA polymerase ζ maintains consistent activity and mutagenicity across a wide range of physiological dNTP concentrations.Nucleic acids research · 2017Article
- Understanding how mismatch repair proteins participate in the repair/anti-recombination decision.FEMS yeast research · 2016Article
- 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
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Mutations are a major driving force of evolution and genetic disease. In eukaryotes, mutations are produced in the chromatin environment, but the impact of chromatin on mutagenesis is poorly understood. Previous studies have determined that in yeast Saccharomyces cerevisiae, Rtt109-dependent acetylation of histone H3 on K56 is an abundant modification that is introduced in chromatin in S phase and removed by Hst3 and Hst4 in G2/M. We show here that the chromatin deacetylation on histone H3 K56 by Hst3 and Hst4 is required for the suppression of spontaneous gross chromosomal rearrangements, base substitutions, 1-bp insertions/deletions, and complex mutations. The rate of base substitutions in hst3Δ hst4Δ is similar to that in isogenic mismatch repair-deficient msh2Δ mutant. We also provide evidence that H3 K56 acetylation by Rtt109 is important for safeguarding DNA from small insertions/deletions and complex mutations. Furthermore, we reveal that both the deacetylation and acetylation on histone H3 K56 are involved in mutation avoidance mechanisms that cooperate with mismatch repair and the proofreading activities of replicative DNA polymerases in suppressing spontaneous mutagenesis. Our results suggest that cyclic acetylation and deacetylation of chromatin contribute to replication fidelity and play important roles in the protection of nuclear DNA from diverse spontaneous mutations.
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