Evidence map›Paper›PMID 30543624›Full record

ArticlePLoS genetics2018

Ribonuclease H1-targeted R-loops in surface antigen gene expression sites can direct trypanosome immune evasion.

Emma Briggs, Kathryn Crouch, Leandro Lemgruber, Craig Lapsley, Richard McCulloch

Abstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. 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
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Regulation of Antigenic Variation byPathogens (Basel, Switzerland) · 2021
    Review
  17. Article
  18. Article
  19. Unpicking the Roles of DNA Damage Protein Kinases in Trypanosomatids.Frontiers in cell and developmental biology · 2021
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Emma BriggsThe Wellcome Centre for Molecular Parasitology, University of Glasgow, College of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, Glasgow, United Kingdom.ORCID 0000-0002-6740-8882
Kathryn CrouchThe Wellcome Centre for Molecular Parasitology, University of Glasgow, College of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, Glasgow, United Kingdom.ORCID 0000-0001-9310-4762
Leandro LemgruberThe Wellcome Centre for Molecular Parasitology, University of Glasgow, College of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, Glasgow, United Kingdom.ORCID 0000-0003-2832-6806
Craig LapsleyThe Wellcome Centre for Molecular Parasitology, University of Glasgow, College of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, Glasgow, United Kingdom.
Richard McCullochThe Wellcome Centre for Molecular Parasitology, University of Glasgow, College of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, Glasgow, United Kingdom.ORCID 0000-0001-5739-976X

Funding

Biotechnology and Biological Sciences Research Council BB/K006495/1Biotechnology and Biological Sciences Research Council BB/M028909/1Biotechnology and Biological Sciences Research Council BB/N016165/1Wellcome Trust 104111
6 · The paper itself

Abstract

Switching of the Variant Surface Glycoprotein (VSG) in Trypanosoma brucei provides a crucial host immune evasion strategy that is catalysed both by transcription and recombination reactions, each operating within specialised telomeric VSG expression sites (ES). VSG switching is likely triggered by events focused on the single actively transcribed ES, from a repertoire of around 15, but the nature of such events is unclear. Here we show that RNA-DNA hybrids, called R-loops, form preferentially within sequences termed the 70 bp repeats in the actively transcribed ES, but spread throughout the active and inactive ES, in the absence of RNase H1, which degrades R-loops. Loss of RNase H1 also leads to increased levels of VSG coat switching and replication-associated genome damage, some of which accumulates within the active ES. This work indicates VSG ES architecture elicits R-loop formation, and that these RNA-DNA hybrids connect T. brucei immune evasion by transcription and recombination.

Indexed as

AnimalsAntigenic VariationDNA DamageGenome, ProtozoanHost-Parasite InteractionsHumansImmune EvasionProtozoan ProteinsRibonuclease HTrypanosoma brucei bruceiTrypanosomiasis, AfricanVariant Surface Glycoproteins, TrypanosomaProtozoan ProteinsRibonuclease Hribonuclease HIVariant Surface Glycoproteins, Trypanosoma

Identifiers

PMID30543624
PMCPMC6292569

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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.