ArticlePLoS genetics2015
Hyper-Acetylation of Histone H3K56 Limits Break-Induced Replication by Inhibiting Extensive Repair Synthesis.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 42 citations in OpenAlex.
- Genome-wide screen reveals dependence of break induced replication on several distinct checkpoints.Nature communications · 2025Article
- Strategic targeting of Cas9 nickase expands tandem gene arrays.Cell genomics · 2025Article
- A Rfa1-MN-based system reveals new factors involved in the rescue of broken replication forks.PLoS genetics · 2025Article
- Stressed? Break-induced replication comes to the rescue!DNA repair · 2024Review
- Article
- Transcription as source of genetic heterogeneity in budding yeast.Yeast (Chichester, England) · 2024Review
- Genetic inhibitors of APOBEC3B-induced mutagenesis.Genome research · 2023Article
- Histone H3 serine-57 is a CHK1 substrate whose phosphorylation affects DNA repair.Nature communications · 2023Article
- Incorporation of a histone mutant with H3K56 site substitution perturbs the replication machinery in mouse embryonic stem cells.Journal of molecular cell biology · 2022Article
- Potential functions of histone H3.3 lysine 56 acetylation in mammals.Epigenetics · 2022Article
- Stimulation of adaptive gene amplification by origin firing under replication fork constraint.Nucleic acids research · 2022Article
- Histone acetylation dynamics in repair of DNA double-strand breaks.Frontiers in genetics · 2022Review
- Molecular dynamics simulations reveal how H3K56 acetylation impacts nucleosome structure to promote DNA exposure for lesion sensing.DNA repair · 2021Article
- R-Loops and Its Chro-Mates: The Strange Case of Dr. Jekyll and Mr. Hyde.International journal of molecular sciences · 2021Review
- Histones on fire: the effect of Dun1 and Mrc1 on origin firing and replication of hyper-acetylated genomes.Current genetics · 2021Review
- Genetic-variant hotspots and hotspot clusters in the human genome facilitating adaptation while increasing instability.Human genomics · 2021Article
- Review
- ALT control, delete: FANCM as an anti-cancer target in Alternative Lengthening of Telomeres.Nucleus (Austin, Tex.) · 2019Review
- Yeast Sirtuin Family Members Maintain Transcription Homeostasis to Ensure Genome Stability.Cell reports · 2019Article
- A synthetic non-histone substrate to study substrate targeting by the Gcn5 HAT and sirtuin HDACs.The Journal of biological chemistry · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Break-induced replication (BIR) has been implicated in restoring eroded telomeres and collapsed replication forks via single-ended invasion and extensive DNA synthesis on the recipient chromosome. Unlike other recombination subtypes, DNA synthesis in BIR likely relies heavily on mechanisms enabling efficient fork progression such as chromatin modification. Herein we report that deletion of HST3 and HST4, two redundant de-acetylases of histone H3 Lysine 56 (H3K56), inhibits BIR, sensitizes checkpoint deficient cells to deoxyribonucleotide triphosphate pool depletion, and elevates translocation-type gross chromosomal rearrangements (GCR). The basis for deficiency in BIR and gene conversion with long gap synthesis in hst3Δ hst4Δ cells can be traced to a defect in extensive DNA synthesis. Distinct from other cellular defects associated with deletion of HST3 and HST4 including thermo-sensitivity and elevated spontaneous mutagenesis, the BIR defect in hst3Δ hst4Δ cannot be offset by the deletion of RAD17 or MMS22, but rather by the loss of RTT109 or ASF1, or in combination with the H3K56R mutation, which also restores tolerance to replication stress in mrc1 mutants. Our studies suggest that acetylation of H3K56 limits extensive repair synthesis and interferes with efficient fork progression in BIR.
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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.