ArticleProceedings of the National Academy of Sciences of the United States of America2003
Saccharomyces cerevisiae chromatin-assembly factors that act during DNA replication function in the maintenance of genome stability.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 138 citations in OpenAlex.
- Multifaceted roles of H2B mono-ubiquitylation in D-loop metabolism during homologous recombination repair.Nucleic acids research · 2025Article
- Signification and Application of Mutator and Antimutator Phenotype-Induced Genetic Variations in Evolutionary Adaptation and Cancer Therapeutics.Journal of microbiology (Seoul, Korea) · 2023Review
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- Reduced histone gene copy number disruptsbioRxiv : the preprint server for biology · 2023Article
- Cac1 WHD and PIP domains have distinct roles in replisome progression and genomic stability.Current genetics · 2021Article
- Dysfunctional CAF-I reveals its role in cell cycle progression and differential regulation of gene silencing.Cell cycle (Georgetown, Tex.) · 2019Article
- MOF Suppresses Replication Stress and Contributes to Resolution of Stalled Replication Forks.Molecular and cellular biology · 2018Article
- Article
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
- Review
- Article
- RRM3 regulates epigenetic conversions in Saccharomyces cerevisiae in conjunction with Chromatin Assembly Factor I.Nucleus (Austin, Tex.) · 2016Article
- Functions of Ubiquitin and SUMO in DNA Replication and Replication Stress.Frontiers in genetics · 2016Review
- Review
- A novel role for the Pol I transcription factor UBTF in maintaining genome stability through the regulation of highly transcribed Pol II genes.Genome research · 2015Article
- Hyper-Acetylation of Histone H3K56 Limits Break-Induced Replication by Inhibiting Extensive Repair Synthesis.PLoS genetics · 2015Article
- The Ddc1-Mec3-Rad17 sliding clamp regulates histone-histone chaperone interactions and DNA replication-coupled nucleosome assembly in budding yeast.The Journal of biological chemistry · 2014Article
- Mutational landscape of yeast mutator strains.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Human CAF-1-dependent nucleosome assembly in a defined system.Cell cycle (Georgetown, Tex.) · 2013Article
- A reversible histone H3 acetylation cooperates with mismatch repair and replicative polymerases in maintaining genome stability.PLoS genetics · 2013Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Some spontaneous gross chromosomal rearrangements (GCRs) seem to result from DNA-replication errors. The chromatin-assembly factor I (CAF-I) and replication-coupling assembly factor (RCAF) complexes function in chromatin assembly during DNA replication and repair and could play a role in maintaining genome stability. Inactivation of CAF-I or RCAF increased the rate of accumulating different types of GCRs including translocations and deletion of chromosome arms with associated de novo telomere addition. Inactivation of CAF-I seems to cause damage that activates the DNA-damage checkpoints, whereas inactivation of RCAF seems to cause damage that activates the DNA-damage and replication checkpoints. Both defects result in increased genome instability that is normally suppressed by these checkpoints, RAD52-dependent recombination, and PIF1-dependent inhibition of de novo telomere addition. Treatment of CAF-I- or RCAF-defective cells with methyl methanesulfonate increased the induction of GCRs compared with that seen for a wild-type strain. These results indicate that coupling of chromatin assembly to DNA replication and DNA repair is critical to maintaining genome stability.
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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.