Evidence map›Paper›PMID 35137208›Full record

ArticleNucleic acids research2022

RAD51 protects against nonconservative DNA double-strand break repair through a nonenzymatic function.

Ayeong So, Elodie Dardillac, Ali Muhammad, Catherine Chailleux, Laura Sesma-Sanz, Sandrine Ragu, Eric Le Cam, Yvan Canitrot, Jean Yves Masson, Pauline Dupaigne and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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  8. International journal of oncology · 2025
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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

12 authors at 2 institutions in 2 countries.

Ayeong SoUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, Equipe Labellisée Ligue Contre le Cancer, France.
Elodie DardillacUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, Equipe Labellisée Ligue Contre le Cancer, France.ORCID 0000-0002-2069-8309
Ali MuhammadGenome Maintenance and Molecular Microscopy UMR 9019 CNRS, Université Paris-Saclay, Gustave Roussy, F-94805, Villejuif Cedex, France.
Catherine ChailleuxCBI, CNRS UMR5088, LBCMCP, Toulouse University, Toulouse, France.
Laura Sesma-SanzGenome Stability Laboratory, CHU de Québec Research Center (Oncology Division), Quebec City, QC, Canada.
Sandrine RaguUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, Equipe Labellisée Ligue Contre le Cancer, France.
Eric Le CamGenome Maintenance and Molecular Microscopy UMR 9019 CNRS, Université Paris-Saclay, Gustave Roussy, F-94805, Villejuif Cedex, France.
Yvan CanitrotCBI, CNRS UMR5088, LBCMCP, Toulouse University, Toulouse, France.
Jean Yves MassonGenome Stability Laboratory, CHU de Québec Research Center (Oncology Division), Quebec City, QC, Canada.
Pauline DupaigneGenome Maintenance and Molecular Microscopy UMR 9019 CNRS, Université Paris-Saclay, Gustave Roussy, F-94805, Villejuif Cedex, France.
Bernard S LopezUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, Equipe Labellisée Ligue Contre le Cancer, France.ORCID 0000-0001-5088-0155
Josée Guirouilh-BarbatUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, Equipe Labellisée Ligue Contre le Cancer, France.
Centre National de la Recherche Scientifique · FRGenome Canada · CA

Funding

CIHR FDN-388879
6 · The paper itself

Abstract

Selection of the appropriate DNA double-strand break (DSB) repair pathway is decisive for genetic stability. It is proposed to act according to two steps: 1-canonical nonhomologous end-joining (C-NHEJ) versus resection that generates single-stranded DNA (ssDNA) stretches; 2-on ssDNA, gene conversion (GC) versus nonconservative single-strand annealing (SSA) or alternative end-joining (A-EJ). Here, we addressed the mechanisms by which RAD51 regulates this second step, preventing nonconservative repair in human cells. Silencing RAD51 or BRCA2 stimulated both SSA and A-EJ, but not C-NHEJ, validating the two-step model. Three different RAD51 dominant-negative forms (DN-RAD51s) repressed GC and stimulated SSA/A-EJ. However, a fourth DN-RAD51 repressed SSA/A-EJ, although it efficiently represses GC. In living cells, the three DN-RAD51s that stimulate SSA/A-EJ failed to load efficiently onto damaged chromatin and inhibited the binding of endogenous RAD51, while the fourth DN-RAD51, which inhibits SSA/A-EJ, efficiently loads on damaged chromatin. Therefore, the binding of RAD51 to DNA, rather than its ability to promote GC, is required for SSA/A-EJ inhibition by RAD51. We showed that RAD51 did not limit resection of endonuclease-induced DSBs, but prevented spontaneous and RAD52-induced annealing of complementary ssDNA in vitro. Therefore, RAD51 controls the selection of the DSB repair pathway, protecting genome integrity from nonconservative DSB repair through ssDNA occupancy, independently of the promotion of CG.

Indexed as

DNA Breaks, Double-StrandedRad51 RecombinaseChromatinDNA End-Joining RepairDNA RepairDNA, Single-StrandedHumansChromatinDNA, Single-StrandedRAD51 protein, humanRad51 Recombinase

Identifiers

PMID35137208
PMCPMC8934640
OpenAlexW4210479033

What OpenQuestion holds

Textmetadata
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.