Evidence map›Paper›PMID 27866150›Full record

ArticleG3 (Bethesda, Md.)2017

CRISPR/Cas9-Induced Double-Strand Break Repair in Arabidopsis Nonhomologous End-Joining Mutants.

Hexi Shen, Gary D Strunks, Bart J P M Klemann, Paul J J Hooykaas, Sylvia de Pater

Open access · goldAbstract read
In one paragraph

Article in G3 (Bethesda, Md.), 2017. 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
2.7field-weighted citation impact, top 9% of its field
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, 59 citations in OpenAlex.

  1. Review
  2. Review
  3. Plant tolerance mechanisms to DNA-damaging UV stress.Journal of experimental botany · 2025
    Review
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  11. Review
  12. Article
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  14. Article
  15. Review
  16. Article
  17. Article
  18. Generation of Gene-Knockout Mongolian Gerbils via CRISPR/Cas9 System.Frontiers in bioengineering and biotechnology · 2020
    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

5 authors at 1 institution in 1 country.

Hexi ShenDepartment of Molecular and Developmental Genetics, Institute of Biology, Leiden University, 2333 BE, The Netherlands.
Gary D StrunksDepartment of Molecular and Developmental Genetics, Institute of Biology, Leiden University, 2333 BE, The Netherlands.
Bart J P M KlemannDepartment of Molecular and Developmental Genetics, Institute of Biology, Leiden University, 2333 BE, The Netherlands.
Paul J J HooykaasDepartment of Molecular and Developmental Genetics, Institute of Biology, Leiden University, 2333 BE, The Netherlands.
Sylvia de PaterDepartment of Molecular and Developmental Genetics, Institute of Biology, Leiden University, 2333 BE, The Netherlands b.s.de.pater@biology.leidenuniv.nl.ORCID 0000-0003-2626-3661
Leiden University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Double-strand breaks (DSBs) are one of the most harmful DNA lesions. Cells utilize two main pathways for DSB repair: homologous recombination (HR) and nonhomologous end-joining (NHEJ). NHEJ can be subdivided into the KU-dependent classical NHEJ (c-NHEJ) and the more error-prone KU-independent backup-NHEJ (b-NHEJ) pathways, involving the poly (ADP-ribose) polymerases (PARPs). However, in the absence of these factors, cells still seem able to adequately maintain genome integrity, suggesting the presence of other b-NHEJ repair factors or pathways independent from KU and PARPs. The outcome of DSB repair by NHEJ pathways can be investigated by using artificial sequence-specific nucleases such as CRISPR/Cas9 to induce DSBs at a target of interest. Here, we used CRISPR/Cas9 for DSB induction at the Arabidopsis cruciferin 3 (CRU3) and protoporphyrinogen oxidase (PPO) genes. DSB repair outcomes via NHEJ were analyzed using footprint analysis in wild-type plants and plants deficient in key factors of c-NHEJ (ku80), b-NHEJ (parp1 parp2), or both (ku80 parp1 parp2). We found that larger deletions of >20 bp predominated after DSB repair in ku80 and ku80 parp1 parp2 mutants, corroborating with a role of KU in preventing DSB end resection. Deletion lengths did not significantly differ between ku80 and ku80 parp1 parp2 mutants, suggesting that a KU- and PARP-independent b-NHEJ mechanism becomes active in these mutants. Furthermore, microhomologies and templated insertions were observed at the repair junctions in the wild type and all mutants. Since these characteristics are hallmarks of polymerase θ-mediated DSB repair, we suggest a possible role for this recently discovered polymerase in DSB repair in plants.

Indexed as

ArabidopsisArabidopsis ProteinsCRISPR-Cas SystemsDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA End-Joining RepairDNA HelicasesDNA RepairGlobulinsHomologous RecombinationMutationPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesProtoporphyrinogen OxidaseSeed Storage ProteinsArabidopsis ProteinsAT4G02390 protein, Arabidopsiscruciferin C, ArabidopsisDNA-Binding ProteinsDNA HelicasesGlobulinsKu80 protein, ArabidopsisPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesProtoporphyrinogen OxidaseSeed Storage ProteinsArabidopsis thalianaCRISPR/Cas9double-strand breakKU80nonhomologous end-joining

Identifiers

PMID27866150
PMCPMC5217109
OpenAlexW2550476372

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.