Evidence map›Paper›PMID 39631395›Full record

ArticleMolecular cell2025

Repair of replication-dependent double-strand breaks differs between the leading and lagging strands.

Michael T Kimble, Aakanksha Sane, Robert J D Reid, Matthew J Johnson, Rodney Rothstein, Lorraine S Symington

Abstract read
In one paragraph

Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

  1. Article
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  8. Review
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  10. Review
  11. Asymmetrical recognition and processing of double-strand breaks formed during DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Mitotic recombination events and single-base mutations induced by ultraviolet light in G1-arrested yeast cells.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025
    Review
  18. Emerging drivers of DNA repeat expansions.Biochemical Society transactions · 2025
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Michael T KimbleProgram in Biological Sciences, Columbia University, New York, NY 10027, USA; Department of Microbiology & Immunology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Aakanksha SaneDepartment of Microbiology & Immunology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Robert J D ReidDepartment of Genetics & Development, Columbia University Irving Medical Center, New York, NY 10032, USA.
Matthew J JohnsonProgram in Biological Sciences, Columbia University, New York, NY 10027, USA; Department of Microbiology & Immunology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Rodney RothsteinDepartment of Genetics & Development, Columbia University Irving Medical Center, New York, NY 10032, USA.
Lorraine S SymingtonDepartment of Microbiology & Immunology, Columbia University Irving Medical Center, New York, NY 10032, USA; Department of Genetics & Development, Columbia University Irving Medical Center, New York, NY 10032, USA. Electronic address: lss5@cumc.columbia.edu.

Funding

Molecular Mechanisms Underlying Recombination at DNA Double-Strand Breaks and Stalled Replication ForksR35GM118180 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Rodney J. ROTHSTEIN · 2016 to 2026
$8.5M
Mechanism and regulation of DNA double-strand break repairR35GM126997 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Lorraine S Symington · 2018 to 2026
$5.9M
Genome and Epigenome Integrity In CancerT32CA265828 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Alberto Ciccia, Chao Lu · 2022 to 2026
$1.8M
NCI NIH HHS T32 CA265828NIGMS NIH HHS R35 GM118180NIGMS NIH HHS R35 GM126997
6 · The paper itself

Abstract

Single-strand breaks (SSBs) are one of the most commonly occurring endogenous lesions with the potential to give rise to cytotoxic double-strand breaks (DSBs) during DNA replication. To investigate how replication-dependent DSBs are repaired, we employed Cas9 nickase (nCas9) to generate site- and strand-specific nicks in the budding yeast genome. We found that nCas9-induced nicks are converted to mostly double-ended DSBs during S phase. Repair of replication-associated DSBs requires homologous recombination (HR) and is independent of classical non-homologous end joining. Consistent with a strong bias to repair these lesions using a sister-chromatid template, we observed minimal induction of inter-chromosomal HR by nCas9. In a genome-wide screen to identify factors necessary for the repair of replication-dependent DSBs, we recovered components of the replication-coupled nucleosome assembly (RCNA) pathway. Our findings suggest that the RCNA pathway is especially important to repair DSBs arising from nicks in the leading-strand template through acetylation of histone H3K56.

Indexed as

DNA Breaks, Double-StrandedDNA ReplicationSaccharomyces cerevisiaeCRISPR-Associated Protein 9CRISPR-Cas SystemsDNA End-Joining RepairDNA, FungalDNA RepairHistonesHomologous RecombinationNucleosomesRecombinational DNA RepairSaccharomyces cerevisiae ProteinsS PhaseCRISPR-Associated Protein 9DNA, FungalHistonesNucleosomesSaccharomyces cerevisiae ProteinsDNA replicationH3K56 acetylationhomologous recombinationMms22Mre11Rad51Rtt109

Identifiers

PMID39631395
PMCPMC11698654

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.