Evidence map›Paper›PMID 31673055›Full record

ArticleScientific reports2019

Genome-scale CRISPR screens are efficient in non-homologous end-joining deficient cells.

Joana Ferreira da Silva, Sejla Salic, Marc Wiedner, Paul Datlinger, Patrick Essletzbichler, Alexander Hanzl, Giulio Superti-Furga, Christoph Bock, Georg Winter, Joanna I Loizou

Abstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Polθ Inhibition: An Anticancer Therapy for HR-Deficient Tumours.International journal of molecular sciences · 2022
    Review
  9. Review
  10. Rational Selection of CRISPR-Cas9 Guide RNAs for Homology-Directed Genome Editing.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  11. Article
  12. Review
  13. Review
  14. 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

10 authors.

Joana Ferreira da SilvaCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
Sejla SalicCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
Marc WiednerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
Paul DatlingerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
Patrick EssletzbichlerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
Alexander HanzlCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
Giulio Superti-FurgaCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.ORCID http://orcid.org/0000-0002-0570-1768
Christoph BockCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.ORCID http://orcid.org/0000-0001-6091-3088
Georg WinterCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria.
Joanna I LoizouCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, AKH BT 25.3, 1090, Vienna, Austria. jloizou@cemm.oeaw.ac.at.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mutagenic repair of Cas9 generated breaks is thought to predominantly rely on non-homologous end-joining (NHEJ), leading to insertions and deletions within DNA that culminate in gene knock-out (KO). In this study, by taking focused as well as genome-wide approaches, we show that this pathway is dispensable for the repair of such lesions. Genetic ablation of NHEJ is fully compensated for by alternative end joining (alt-EJ), in a POLQ-dependent manner, resulting in a distinct repair signature with larger deletions that may be exploited for large-scale genome editing. Moreover, we show that cells deficient for both NHEJ and alt-EJ were still able to repair CRISPR-mediated DNA double-strand breaks, highlighting how little is yet known about the mechanisms of CRISPR-based genome editing.

Indexed as

Cell LineCRISPR-Associated Protein 9CRISPR-Cas SystemsDNA Breaks, Double-StrandedDNA End-Joining RepairGene EditingGene Knockout TechniquesHSP90 Heat-Shock ProteinsHumansRNA, Guide, CRISPR-Cas SystemsUbiquitin-Protein LigasesCRISPR-Associated Protein 9HSP90AA1 protein, humanHSP90 Heat-Shock ProteinsRNA, Guide, CRISPR-Cas SystemsRNF152 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID31673055
PMCPMC6823505

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LicenceCC BY
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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.