ArticleMolecular and cellular biology2012
Histone H3 lysine 56 acetylation and the response to DNA replication fork damage.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 86 citations in OpenAlex.
- Identifying critical lysines in mammalian histone H3 with high-throughput CRISPR prime editing.Nature genetics · 2026Article
- Replication stress induced exposure to methotrexate in root meristem cells of Vicia faba.Histochemistry and cell biology · 2026Article
- Biosynthesis, Regulation, and Biotechnological Production Strategies of Riboflavin (Vitamin BPharmaceuticals (Basel, Switzerland) · 2026Review
- Integrated dual transcriptome sequencing and experimental validation reveal potential mechanisms of baicalin againstFrontiers in microbiology · 2026Article
- A Rfa1-MN-based system reveals new factors involved in the rescue of broken replication forks.PLoS genetics · 2025Article
- Oxidative replication stress induced by long-term exposure to hydroxyurea in root meristem cells of Vicia faba.Plant cell reports · 2024Article
- Functional analysis of chromatin-associated proteins in Sordaria macrospora reveals similar roles for RTT109 and ASF1 in development and DNA damage response.G3 (Bethesda, Md.) · 2024Article
- Article
- Chromatin assembly factor-1 preserves genome stability inCell stress · 2023Article
- Histone H3 serine-57 is a CHK1 substrate whose phosphorylation affects DNA repair.Nature communications · 2023Article
- The Role of Histone Modification in DNA Replication-Coupled Nucleosome Assembly and Cancer.International journal of molecular sciences · 2023Review
- The Chromatin Landscape around DNA Double-Strand Breaks in Yeast and Its Influence on DNA Repair Pathway Choice.International journal of molecular sciences · 2023Review
- Persistent Acetylation of Histone H3 Lysine 56 Compromises the Activity of DNA Replication Origins.Molecular and cellular biology · 2023Article
- 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
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- Starvation-induced proteasome assemblies in the nucleus link amino acid supply to apoptosis.Nature communications · 2021Article
- Molecular dynamics simulations reveal how H3K56 acetylation impacts nucleosome structure to promote DNA exposure for lesion sensing.DNA repair · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
In Saccharomyces cerevisiae, histone H3 lysine 56 acetylation (H3K56ac) occurs in newly synthesized histones that are deposited throughout the genome during DNA replication. Defects in H3K56ac sensitize cells to genotoxic agents, suggesting that this modification plays an important role in the DNA damage response. However, the links between histone acetylation, the nascent chromatin structure, and the DNA damage response are poorly understood. Here we report that cells devoid of H3K56ac are sensitive to DNA damage sustained during transient exposure to methyl methanesulfonate (MMS) or camptothecin but are only mildly affected by hydroxyurea. We demonstrate that, after exposure to MMS, H3K56ac-deficient cells cannot complete DNA replication and eventually segregate chromosomes with intranuclear foci containing the recombination protein Rad52. In addition, we provide evidence that these phenotypes are not due to defects in base excision repair, defects in DNA damage tolerance, or a lack of Rad51 loading at sites of DNA damage. Our results argue that the acute sensitivity of H3K56ac-deficient cells to MMS and camptothecin stems from a failure to complete the repair of specific types of DNA lesions by recombination and/or from defects in the completion of DNA replication.
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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.