Evidence map›Paper›PMID 26077599›Full record

ArticleNature communications2015

Polymerase Θ is a key driver of genome evolution and of CRISPR/Cas9-mediated mutagenesis.

Robin van Schendel, Sophie F Roerink, Vincent Portegijs, Sander van den Heuvel, Marcel Tijsterman

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

65 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Disruption of Microhomology-mediated End-joining in Ewing Sarcoma.bioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Multifaceted Nature of DNA Polymerase θ.International journal of molecular sciences · 2023
    Review
  17. Gene editing in the nematode parasiteFrontiers in parasitology · 2023
    Article
  18. Article
  19. Article
  20. Review

5 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Robin van SchendelDepartment of Human Genetics, Leiden University Medical Center, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Sophie F RoerinkDepartment of Human Genetics, Leiden University Medical Center, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Vincent PortegijsDepartment of Biology, Division of Developmental Biology, Utrecht University, Padualaan 8, 3584 CH, Utrecht, The Netherlands.
Sander van den HeuvelDepartment of Biology, Division of Developmental Biology, Utrecht University, Padualaan 8, 3584 CH, Utrecht, The Netherlands.
Marcel TijstermanDepartment of Human Genetics, Leiden University Medical Center, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Leiden University Medical Center · NLUtrecht University · NL

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
European Research Council 203379NIH HHS P40 OD010440
6 · The paper itself

Abstract

Cells are protected from toxic DNA double-stranded breaks (DSBs) by a number of DNA repair mechanisms, including some that are intrinsically error prone, thus resulting in mutations. To what extent these mechanisms contribute to evolutionary diversification remains unknown. Here, we demonstrate that the A-family polymerase theta (POLQ) is a major driver of inheritable genomic alterations in Caenorhabditis elegans. Unlike somatic cells, which use non-homologous end joining (NHEJ) to repair DNA transposon-induced DSBs, germ cells use polymerase theta-mediated end joining, a conceptually simple repair mechanism requiring only one nucleotide as a template for repair. Also CRISPR/Cas9-induced genomic changes are exclusively generated through polymerase theta-mediated end joining, refuting a previously assumed requirement for NHEJ in their formation. Finally, through whole-genome sequencing of propagated populations, we show that only POLQ-proficient animals accumulate genomic scars that are abundantly present in genomes of wild C. elegans, pointing towards POLQ as a major driver of genome diversification.

Indexed as

CRISPR-Cas SystemsDNA End-Joining RepairMutagenesisAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA Breaks, Double-StrandedDNA-Directed DNA PolymeraseDNA Polymerase thetaDNA RepairEvolution, MolecularGenome, HelminthGerm CellsGerm-Line MutationMutationCaenorhabditis elegans ProteinsDNA-Directed DNA PolymeraseDNA Polymerase theta

Identifiers

PMID26077599
PMCPMC4490562
OpenAlexW2254550535

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.