Evidence map›Paper›PMID 25313826›Full record

ArticlePLoS biology2014

The chromatin assembly factor 1 promotes Rad51-dependent template switches at replication forks by counteracting D-loop disassembly by the RecQ-type helicase Rqh1.

Violena Pietrobon, Karine Fréon, Julien Hardy, Audrey Costes, Ismail Iraqui, Françoise Ochsenbein, Sarah A E Lambert

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 28% of its field
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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  6. A marker-free genome editing method inmicroPublication biology · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. ATRX and RECQ5 define distinct homologous recombination subpathways.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Review
  12. Review
  13. Article
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  15. Article
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  18. Monoubiquitylation of histone H2B contributes to the bypass of DNA damage during and after DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  19. Review
  20. Article
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 at 2 institutions in 1 country.

Violena PietrobonInstitut Curie, Centre de Recherche, Orsay, France; Centre national de la Recherche Scientifique, UMR3348, Centre Universitaire, Orsay, France.
Karine FréonInstitut Curie, Centre de Recherche, Orsay, France; Centre national de la Recherche Scientifique, UMR3348, Centre Universitaire, Orsay, France.
Julien HardyInstitut Curie, Centre de Recherche, Orsay, France; Centre national de la Recherche Scientifique, UMR3348, Centre Universitaire, Orsay, France.
Audrey CostesInstitut Curie, Centre de Recherche, Orsay, France; Centre national de la Recherche Scientifique, UMR3348, Centre Universitaire, Orsay, France.
Ismail IraquiInstitut Curie, Centre de Recherche, Orsay, France; Centre national de la Recherche Scientifique, UMR3348, Centre Universitaire, Orsay, France.
Françoise OchsenbeinCommissariat à l'Energie Atomique, iBiTec-S, Service de Biologie Intégrative et de Génétique Moléculaire, Gif-sur-Yvette, France.
Sarah A E LambertInstitut Curie, Centre de Recherche, Orsay, France; Centre national de la Recherche Scientifique, UMR3348, Centre Universitaire, Orsay, France.
Institut Curie · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At blocked replication forks, homologous recombination mediates the nascent strands to switch template in order to ensure replication restart, but faulty template switches underlie genome rearrangements in cancer cells and genomic disorders. Recombination occurs within DNA packaged into chromatin that must first be relaxed and then restored when recombination is completed. The chromatin assembly factor 1, CAF-1, is a histone H3-H4 chaperone involved in DNA synthesis-coupled chromatin assembly during DNA replication and DNA repair. We reveal a novel chromatin factor-dependent step during replication-coupled DNA repair: Fission yeast CAF-1 promotes Rad51-dependent template switches at replication forks, independently of the postreplication repair pathway. We used a physical assay that allows the analysis of the individual steps of template switch, from the recruitment of recombination factors to the formation of joint molecules, combined with a quantitative measure of the resulting rearrangements. We reveal functional and physical interplays between CAF-1 and the RecQ-helicase Rqh1, the BLM homologue, mutations in which cause Bloom's syndrome, a human disease associating genome instability with cancer predisposition. We establish that CAF-1 promotes template switch by counteracting D-loop disassembly by Rqh1. Consequently, the likelihood of faulty template switches is controlled by antagonistic activities of CAF-1 and Rqh1 in the stability of the D-loop. D-loop stabilization requires the ability of CAF-1 to interact with PCNA and is thus linked to the DNA synthesis step. We propose that CAF-1 plays a regulatory role during template switch by assembling chromatin on the D-loop and thereby impacting the resolution of the D-loop.

Indexed as

DNA ReplicationHomologous RecombinationDNA HelicasesDNA RepairGenome, FungalNuclear ProteinsProliferating Cell Nuclear AntigenRad51 RecombinaseSchizosaccharomycesSchizosaccharomyces pombe ProteinsDNA HelicasesHba1 protein, S pombeNuclear ProteinsProliferating Cell Nuclear AntigenRad51 RecombinaseRHP51 protein, S pombeRqh1 protein, S pombeSchizosaccharomyces pombe Proteins

Identifiers

PMID25313826
PMCPMC4196752
OpenAlexW2027065836

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.