Evidence map›Paper›PMID 17693593›Full record

ArticleEukaryotic cell2007

Ku heterodimer-independent end joining in Trypanosoma brucei cell extracts relies upon sequence microhomology.

Peter Burton, David J McBride, Jonathan M Wilkes, J David Barry, Richard McCulloch

Open access · diamondAbstract read
In one paragraph

Article in Eukaryotic cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

44 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Telomere maintenance in African trypanosomes.Frontiers in molecular biosciences · 2023
    Review
  7. Genome Protection by DNA Polymerase θ.Annual review of genetics · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Unpicking the Roles of DNA Damage Protein Kinases in Trypanosomatids.Frontiers in cell and developmental biology · 2021
    Review
  13. Review
  14. DNA Double-Strand Breaks: A Double-Edged Sword for Trypanosomatids.Frontiers in cell and developmental biology · 2021
    Review
  15. Article
  16. Review
  17. Efficient Single-Gene and Gene Family Editing in the Apicomplexan ParasiteFrontiers in bioengineering and biotechnology · 2020
    Article
  18. ATR Kinase Is a Crucial Player Mediating the DNA Damage Response inFrontiers in cell and developmental biology · 2020
    Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Peter BurtonThe Wellcome Centre for Molecular Parasitology, University of Glasgow, Glasgow Biomedical Research Centre, Glasgow, Scotland, UK.
David J McBride
Jonathan M Wilkes
J David Barry
Richard McCulloch
Wellcome Centre for Molecular Parasitology · GBUniversity of Glasgow · GB

Funding

Medical Research Council G0401553Wellcome Trust
6 · The paper itself

Abstract

DNA double-strand breaks (DSBs) are repaired primarily by two distinct pathways: homologous recombination and nonhomologous end joining (NHEJ). NHEJ has been found in all eukaryotes examined to date and has been described recently for some bacterial species, illustrating its ancestry. Trypanosoma brucei is a divergent eukaryotic protist that evades host immunity by antigenic variation, a process in which homologous recombination plays a crucial function. While homologous recombination has been examined in some detail in T. brucei, little work has been done to examine what other DSB repair pathways the parasite utilizes. Here we show that T. brucei cell extracts support the end joining of linear DNA molecules. These reactions are independent of the Ku heterodimer, indicating that they are distinct from NHEJ, and are guided by sequence microhomology. We also demonstrate bioinformatically that T. brucei, in common with other kinetoplastids, does not encode recognizable homologues of DNA ligase IV or XRCC4, suggesting that NHEJ is either absent or mechanistically diverged in these pathogens.

Indexed as

Cell ExtractsSequence Homology, Nucleic AcidAdenosine TriphosphateAnimalsAntigens, NuclearBase SequenceCatalysisCell NucleusConserved SequenceDimerizationDNA-Binding ProteinsDNA, ProtozoanKu AutoantigenMagnesiumMolecular Sequence DataPhylogenyAdenosine TriphosphateAntigens, NuclearCell ExtractsDNA-Binding ProteinsDNA, ProtozoanKu AutoantigenMagnesiumRad51 Recombinase

Identifiers

PMID17693593
PMCPMC2043400
OpenAlexW2121260097

What OpenQuestion holds

Textmetadata
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.