Evidence map›Paper›PMID 33067475›Full record

ArticleNature communications2020

Repair of G1 induced DNA double-strand breaks in S-G2/M by alternative NHEJ.

Wei Yu, Chloé Lescale, Loelia Babin, Marie Bedora-Faure, Hélène Lenden-Hasse, Ludivine Baron, Caroline Demangel, José Yelamos, Erika Brunet, Ludovic Deriano

Abstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Article
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  4. CRISPR Gene Tagging for Illuminating Endogenous Protein Dynamics.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
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  10. Article
  11. Review
  12. Review
  13. Assessment and Mitigation of CRISPR-Cas9-Induced Nontargeted Translocations.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  14. Article
  15. Article
  16. Review
  17. Article
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  19. Article
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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

10 authors.

Wei YuGenome Integrity, Immunity and Cancer Unit, Equipe Labellisée Ligue Contre Le Cancer, Institut Pasteur, 75015, Paris, France.
Chloé LescaleGenome Integrity, Immunity and Cancer Unit, Equipe Labellisée Ligue Contre Le Cancer, Institut Pasteur, 75015, Paris, France.ORCID 0000-0003-0622-1149
Loelia BabinGenome Dynamics in the Immune System Laboratory, Equipe Labellisée Ligue Contre Le Cancer, INSERM UMR 1163, Université Paris Descartes Sorbonne Paris Cité, Institut Imagine, 75015, Paris, France.
Marie Bedora-FaureGenome Integrity, Immunity and Cancer Unit, Equipe Labellisée Ligue Contre Le Cancer, Institut Pasteur, 75015, Paris, France.
Hélène Lenden-HasseGenome Integrity, Immunity and Cancer Unit, Equipe Labellisée Ligue Contre Le Cancer, Institut Pasteur, 75015, Paris, France.
Ludivine BaronImmunobiology of Infection Unit, INSERM U1221, Institut Pasteur, 75015, Paris, France.
Caroline DemangelImmunobiology of Infection Unit, INSERM U1221, Institut Pasteur, 75015, Paris, France.
José YelamosCancer Research Program, Hospital del Mar Medical Research Institute, 08003, Barcelona, Spain.ORCID 0000-0003-1195-1496
Erika BrunetGenome Dynamics in the Immune System Laboratory, Equipe Labellisée Ligue Contre Le Cancer, INSERM UMR 1163, Université Paris Descartes Sorbonne Paris Cité, Institut Imagine, 75015, Paris, France.
Ludovic DerianoGenome Integrity, Immunity and Cancer Unit, Equipe Labellisée Ligue Contre Le Cancer, Institut Pasteur, 75015, Paris, France. ludovic.deriano@pasteur.fr.ORCID 0000-0002-9673-9525

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The alternative non-homologous end-joining (NHEJ) pathway promotes DNA double-strand break (DSB) repair in cells deficient for NHEJ or homologous recombination, suggesting that it operates at all stages of the cell cycle. Here, we use an approach in which DNA breaks can be induced in G1 cells and their repair tracked, enabling us to show that joining of DSBs is not functional in G1-arrested XRCC4-deficient cells. Cell cycle entry into S-G2/M restores DSB repair by Pol θ-dependent and PARP1-independent alternative NHEJ with repair products bearing kilo-base long DNA end resection, micro-homologies and chromosome translocations. We identify a synthetic lethal interaction between XRCC4 and Pol θ under conditions of G1 DSBs, associated with accumulation of unresolved DNA ends in S-G2/M. Collectively, our results support the conclusion that the repair of G1 DSBs progressing to S-G2/M by alternative NHEJ drives genomic instability and represent an attractive target for future DNA repair-based cancer therapies.

Indexed as

Cell CycleDNA Breaks, Double-StrandedDNA End-Joining RepairAnimalsDNA-Binding ProteinsG1 PhaseMicePoly (ADP-Ribose) Polymerase-1DNA-Binding ProteinsParp1 protein, mousePoly (ADP-Ribose) Polymerase-1XRCC4 protein, mouse

Identifiers

PMID33067475
PMCPMC7567796

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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.