Evidence map›Paper›PMID 22952449›Full record

ArticlePLoS pathogens2012

Telomere length affects the frequency and mechanism of antigenic variation in Trypanosoma brucei.

Galadriel A Hovel-Miner, Catharine E Boothroyd, Monica Mugnier, Oliver Dreesen, George A M Cross, F Nina Papavasiliou

Abstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed.

  1. Microbiology spectrum · 2026
    Article
  2. Article
  3. Review
  4. RAD51-mediated R-loop formation acts to repair transcription-associated DNA breaks driving antigenic variation inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Article
  6. Article
  7. Telomere maintenance in African trypanosomes.Frontiers in molecular biosciences · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Regulation of Antigenic Variation byPathogens (Basel, Switzerland) · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. DNA Double-Strand Breaks: A Double-Edged Sword for Trypanosomatids.Frontiers in cell and developmental biology · 2021
    Review
  19. Science advances · 2020
    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

6 authors.

Galadriel A Hovel-MinerLaboratory of Lymphocyte Biology, The Rockefeller University, New York, New York, United States of America.
Catharine E Boothroyd
Monica Mugnier
Oliver Dreesen
George A M Cross
F Nina Papavasiliou

Funding

MOLECULAR GENETICS OF TRYPANOSOME ANTIGENIC VARIATIONR01AI021729 · NIAID · ROCKEFELLER UNIVERSITY · PI CROSS, GEORGE ALAN MARTIN · 1985 to 2011
$5.3M
Parameters that govern initiation of VSG switching in T.bruceiR01AI085973 · NIAID · ROCKEFELLER UNIVERSITY · PI PAPAVASILIOU, F. NINA · 2010 to 2014
$2.1M
MOLECULAR GENETICS OF TRYPANOSOME ANTIGENIC VARIATIONR37AI021729 · NIAID · ROCKEFELLER UNIVERSITY · PI CROSS, GEORGE ALAN MARTIN · 1988 to 1997
–
NIAID NIH HHS AI085973NIAID NIH HHS AI21729NIAID NIH HHS R01 AI021729NIAID NIH HHS R01 AI085973
6 · The paper itself

Abstract

Trypanosoma brucei is a master of antigenic variation and immune response evasion. Utilizing a genomic repertoire of more than 1000 Variant Surface Glycoprotein-encoding genes (VSGs), T. brucei can change its protein coat by "switching" from the expression of one VSG to another. Each active VSG is monoallelically expressed from only one of approximately 15 subtelomeric sites. Switching VSG expression occurs by three predominant mechanisms, arguably the most significant of which is the non-reciprocal exchange of VSG containing DNA by duplicative gene conversion (GC). How T. brucei orchestrates its complex switching mechanisms remains to be elucidated. Recent work has demonstrated that an exogenous DNA break in the active site could initiate a GC based switch, yet the source of the switch-initiating DNA lesion under natural conditions is still unknown. Here we investigated the hypothesis that telomere length directly affects VSG switching. We demonstrate that telomerase deficient strains with short telomeres switch more frequently than genetically identical strains with long telomeres and that, when the telomere is short, switching preferentially occurs by GC. Our data supports the hypothesis that a short telomere at the active VSG expression site results in an increase in subtelomeric DNA breaks, which can initiate GC based switching. In addition to their significance for T. brucei and telomere biology, the findings presented here have implications for the many diverse pathogens that organize their antigenic genes in subtelomeric regions.

Indexed as

Genetic VariationAntigenic VariationDNA, ProtozoanGene ConversionGene DuplicationHumansPhenotypeTelomeraseTelomereTelomere HomeostasisTrypanosoma brucei bruceiVariant Surface Glycoproteins, TrypanosomaDNA, ProtozoanTelomeraseVariant Surface Glycoproteins, Trypanosoma

Identifiers

PMID22952449
PMCPMC3431348

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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.