Evidence map›Paper›PMID 41298353›Full record

ArticleNature communications2025

Polymerase theta repairs persistent G1-induced DNA breaks in S-phase during class switch recombination.

Timea Marton, Jinglong Wang, Amaury Vaysse, Wei Yu, Pierre-Henri Commere, Quentin Holleville, Tristan Espie-Caullet, Richard Frock, Ludovic Deriano

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. 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

9 authors.

Timea MartonInstitut Pasteur, Université Paris Cité, INSERM U1223, Équipe Labellisée Ligue Contre Le Cancer, Genome Integrity, Immunity and Cancer Unit, Paris, France.
Jinglong WangDepartment of Radiation Oncology, School of Medicine, Stanford University, Stanford, CA, USA.
Amaury VaysseInstitut Pasteur, Université Paris Cité, INSERM U1223, Équipe Labellisée Ligue Contre Le Cancer, Genome Integrity, Immunity and Cancer Unit, Paris, France.ORCID http://orcid.org/0000-0003-2397-4230
Wei YuInstitut Pasteur, Université Paris Cité, INSERM U1223, Équipe Labellisée Ligue Contre Le Cancer, Genome Integrity, Immunity and Cancer Unit, Paris, France.ORCID http://orcid.org/0000-0002-1777-5254
Pierre-Henri CommereFlow Cytometry Platform, Institut Pasteur, Université Paris Cité, Paris, France.
Quentin HollevilleInstitut Pasteur, Université Paris Cité, INSERM U1223, Équipe Labellisée Ligue Contre Le Cancer, Genome Integrity, Immunity and Cancer Unit, Paris, France.
Tristan Espie-CaulletInstitut Pasteur, Université Paris Cité, INSERM U1223, Équipe Labellisée Ligue Contre Le Cancer, Genome Integrity, Immunity and Cancer Unit, Paris, France.ORCID http://orcid.org/0000-0003-1977-8982
Richard FrockDepartment of Radiation Oncology, School of Medicine, Stanford University, Stanford, CA, USA.ORCID http://orcid.org/0000-0001-6963-4931
Ludovic DerianoInstitut Pasteur, Université Paris Cité, INSERM U1223, Équipe Labellisée Ligue Contre Le Cancer, Genome Integrity, Immunity and Cancer Unit, Paris, France. lderiano@pasteur.fr.ORCID http://orcid.org/0000-0002-9673-9525

Funding

Agence Nationale de la Recherche (French National Research Agency) CSR_BreakIRAmerican Cancer Society (American Cancer Society, Inc.) RSG-23- 1038994-01DMCInstitut National Du Cancer (French National Cancer Institute) INCa_13852Ligue Contre le Cancer Labellisation 2019-2023 and 2024-2026Wellcome TrustWorldwide Cancer Research 19-0333
6 · The paper itself

Abstract

Non-homologous end joining (NHEJ) is the primary pathway for repairing G1 phase-induced DNA double-strand breaks (DSBs) during immunoglobulin heavy chain (Igh) class switch recombination (CSR) in B lymphocytes. In B cells lacking NHEJ (XRCC4) or DSB end protection (SHLD1), end joining during CSR proceeds through an alternative end-joining pathway. Polymerase theta (Pol θ) is widely regarded as a mediator of this pathway, essential for repairing replication-associated DSBs during mitosis when homologous recombination is unavailable. In this study, we examined CSR in primary B cells lacking XRCC4, SHLD1, and/or Pol θ, revealing two repair pathways: Pol θ-independent productive switching and Pol θ-dependent unproductive switching characterized by end resection, inversion and microhomology. Furthermore, we show that Pol θ-mediated repair under NHEJ-deficiency coincides with G1-to-S phase transition and occurs independently of RHINO and PLK1. Thus, in the absence of NHEJ, Pol θ repairs persistent G1-phase DSBs during S-phase rather than mitosis.

Indexed as

DNA Breaks, Double-StrandedDNA-Directed DNA PolymeraseDNA End-Joining RepairG1 PhaseImmunoglobulin Class SwitchingS PhaseAnimalsB-LymphocytesCell Cycle ProteinsDNA-Binding ProteinsDNA Polymerase thetaEndonucleasesMiceMice, Inbred C57BLMice, KnockoutNuclear ProteinsCell Cycle ProteinsDclre1c protein, mouseDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA Polymerase thetaEndonucleasesNuclear ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsXRCC4 protein, mouse

Identifiers

PMID41298353
PMCPMC12657980

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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.