Evidence map›Paper›PMID 32796846›Full record

ArticleNature communications2020

A scalable CRISPR/Cas9-based fluorescent reporter assay to study DNA double-strand break repair choice.

Paris Roidos, Stephanie Sungalee, Salvatore Benfatto, Özdemirhan Serçin, Adrian M Stütz, Amir Abdollahi, Jan Mauer, Frank T Zenke, Jan O Korbel, Balca R Mardin

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. ALK Knock-In Reporter Reveals APE1 as a Negative Regulator ofInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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.

Paris Roidos *BioMed X Institute (GmbH), Im Neuenheimer Feld 583, Heidelberg, 69120, Germany.ORCID http://orcid.org/0000-0002-6896-8443
Stephanie Sungalee *European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany.
Salvatore BenfattoBioMed X Institute (GmbH), Im Neuenheimer Feld 583, Heidelberg, 69120, Germany.ORCID http://orcid.org/0000-0003-4439-3136
Özdemirhan SerçinBioMed X Institute (GmbH), Im Neuenheimer Feld 583, Heidelberg, 69120, Germany.
Adrian M StützEuropean Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany.
Amir AbdollahiDivision of Molecular and Translational Radiation Oncology, National Centre for Tumour Diseases (NCT), Heidelberg University Hospital, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-8016-5897
Jan MauerBioMed X Institute (GmbH), Im Neuenheimer Feld 583, Heidelberg, 69120, Germany.ORCID http://orcid.org/0000-0002-0189-5876
Frank T ZenkeTranslational Innovation Platform Oncology, Merck KGaA, Darmstadt, Germany.ORCID http://orcid.org/0000-0002-2226-3755
Jan O KorbelEuropean Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-2798-3794
Balca R MardinBioMed X Institute (GmbH), Im Neuenheimer Feld 583, Heidelberg, 69120, Germany. mardin@bio.mx.ORCID http://orcid.org/0000-0002-3903-9354

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Double-strand breaks (DSBs) are the most toxic type of DNA lesions. Cells repair these lesions using either end protection- or end resection-coupled mechanisms. To study DSB repair choice, we present the Color Assay Tracing-Repair (CAT-R) to simultaneously quantify DSB repair via end protection and end resection pathways. CAT-R introduces DSBs using CRISPR/Cas9 in a tandem fluorescent reporter, whose repair distinguishes small insertions/deletions from large deletions. We demonstrate CAT-R applications in chemical and genetic screens. First, we evaluate 21 compounds currently in clinical trials which target the DNA damage response. Second, we examine how 417 factors involved in DNA damage response influence the choice between end protection and end resection. Finally, we show that impairing nucleotide excision repair favors error-free repair, providing an alternative way for improving CRISPR/Cas9-based knock-ins. CAT-R is a high-throughput, versatile assay to assess DSB repair choice, which facilitates comprehensive studies of DNA repair and drug efficiency testing.

Indexed as

Clustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsDNA Breaks, Double-StrandedDNA RepairAtaxia Telangiectasia Mutated ProteinsCell CycleCell SurvivalDNA DamageDNA End-Joining RepairDrug Evaluation, PreclinicalGene Knockout TechniquesHEK293 CellsHumansPoly (ADP-Ribose) Polymerase-1Ataxia Telangiectasia Mutated ProteinsATM protein, humanPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1

Identifiers

PMID32796846
PMCPMC7429917

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.