Evidence map›Paper›PMID 41297802›Full record

ArticleNucleic acids research2025

The histone chaperone CAF-1 prevents homologous recombination-mediated instability of the budding yeast ribosomal DNA during replication-coupled DNA double-strand break repair.

Hajime Futami, Tsugumi Yamaji, Yuko Katayama, Nanase Arata, Mio Nagura, Takehiko Kobayashi, Mariko M Sasaki

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Hajime FutamiLaboratory of Genome Regeneration, Institute for Quantitative Biosciences (IQB), The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
Tsugumi YamajiLaboratory of Gene Quantity Biology, Center for Frontier Research, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan.
Yuko KatayamaLaboratory of Gene Quantity Biology, Center for Frontier Research, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan.
Nanase ArataLaboratory of Gene Quantity Biology, Center for Frontier Research, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan.
Mio NaguraLaboratory of Gene Quantity Biology, Center for Frontier Research, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan.
Takehiko KobayashiLaboratory of Genome Regeneration, Institute for Quantitative Biosciences (IQB), The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.ORCID 0000-0002-7990-3741
Mariko M SasakiLaboratory of Gene Quantity Biology, Center for Frontier Research, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan.ORCID 0000-0003-4208-1251

Funding

Core Research for Evolutional Science and Technology JPMJCR19S3FOREST JPMJFR214PFusion Oriented REsearch for disruptive Science and TechnologyJapan Agency for Medical Research and Development JP21gm1110010Japan Society for the Promotion of Science 17H01443Japan Society for the Promotion of Science 20H05382Japan Society for the Promotion of Science 21H04761Japan Society for the Promotion of Science 24K09417Naito FoundationResearch Organization of Information and SystemsTakeda Science Foundation
6 · The paper itself

Abstract

DNA replication-coupled chromatin assembly is crucial to maintain genome integrity. Here, we demonstrate that the absence of the budding yeast histone chaperone CAF-1 induces the production of extrachromosomal ribosomal RNA gene (rDNA) circles (ERCs), accompanied by chromosomal rDNA copy number changes, in a manner dependent on Fob1-mediated DNA replication fork arrest in the rDNA, the homologous recombination (HR) protein Rad52, and its interaction with proliferating cell nuclear antigen. In the caf-1 mutant, ERC production is triggered partly by increased transcription from the regulatory promoter E-pro, but is also affected by defects independent of E-pro misregulation. Absence of CAF-1 accumulates resected DNA double-strand breaks (DSBs) formed at arrested replication forks, repair of which leads to enhanced ERC formation. CAF-1 deficiency causes partial defects in lagging strand synthesis coupled to nucleosome spacing in the rDNA. Our findings suggest that CAF-1 suppresses HR-mediated rDNA instability during repair of replication-coupled DSBs.

Indexed as

DNA Breaks, Double-StrandedDNA RepairDNA ReplicationDNA, RibosomalHistone ChaperonesHomologous RecombinationRecombinational DNA RepairSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA-Binding ProteinsProliferating Cell Nuclear AntigenRad52 DNA Repair and Recombination ProteinDNA-Binding ProteinsDNA, RibosomalFOB1 protein, S cerevisiaeHistone ChaperonesProliferating Cell Nuclear AntigenRad52 DNA Repair and Recombination ProteinRAD52 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID41297802
PMCPMC12657057

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Registered trials

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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.