ArticleProceedings of the National Academy of Sciences of the United States of America2009
Chromatin assembly factors Asf1 and CAF-1 have overlapping roles in deactivating the DNA damage checkpoint when DNA repair is complete.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 108 citations in OpenAlex.
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- Arp2/3 and type-I myosins control chromosome mobility and end-resection at double-strand breaks in S. cerevisiae.Nature communications · 2025Article
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction.Nucleic acids research · 2025Article
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction.bioRxiv : the preprint server for biology · 2024Article
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- Multilevel interrogation of H3.3 reveals a primordial role in transcription regulation.Epigenetics & chromatin · 2023Article
- The Anaphase-Promoting Complex/Cyclosome Is a Cellular Ageing Regulator.International journal of molecular sciences · 2022Review
- Molecular mechanisms underlying the emergence of polygenetic antifungal drug resistance inJAC-antimicrobial resistance · 2022Article
- Chaperoning histones at the DNA repair dance.DNA repair · 2021Review
- Histone and Chromatin Dynamics Facilitating DNA repair.DNA repair · 2021Review
- Local nucleosome dynamics and eviction following a double-strand break are reversible by NHEJ-mediated repair in the absence of DNA replication.Genome research · 2021Article
- New Methodologies to Study DNA Repair Processes in Space and Time Within Living Cells.Frontiers in cell and developmental biology · 2021Review
- CAF-1 and Rtt101p function within the replication-coupled chromatin assembly network to promote H4 K16ac, preventing ectopic silencing.PLoS genetics · 2020Article
- Functional crosstalk between mTORC1/p70S6K pathway and heterochromatin organization in stress-induced senescence of MSCs.Stem cell research & therapy · 2020Article
- Chromatin regulation and dynamics in stem cells.Current topics in developmental biology · 2020Review
- KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization.iScience · 2019Article
- Dysfunctional CAF-I reveals its role in cell cycle progression and differential regulation of gene silencing.Cell cycle (Georgetown, Tex.) · 2019Article
- Article
- Modulation of Gene Silencing by Cdc7p via H4 K16 Acetylation and Phosphorylation of Chromatin Assembly Factor CAF-1 inGenetics · 2019Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In response to a DNA double-strand break (DSB), chromatin is rapidly modified by the damage dependent checkpoint kinases. Also, disassembly of chromatin occurs at the break site. The damage-induced modification of chromatin structure is involved in the maintenance of the checkpoint. However, it has not been determined how chromatin is restored to its undamaged state when DSB repair is complete. Here, we show the involvement of two chromatin assembly factors (CAFs), Asf1 and CAF-1, in turning off the DNA damage checkpoint in budding yeast. DSB repair or formation of gamma-H2AX does not depend on either the CAF-1 protein, Cac1, or Asf1. Absence of these proteins does not impair the ability of cells to resume cell cycle progression in the presence of an unrepaired DSB (adaptation). However, recovery from cell cycle checkpoint arrest when the DSB is repaired by gene conversion is substantially defective in the absence of both CAF-1 and Asf1, whereas deleting CAC1 or ASF1 individually had little effect. We suggest that CAF-1 and Asf1 function redundantly to deactivate the checkpoint by restoring chromatin structure on the completion of DSB repair.
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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.