Evidence map›Paper›PMID 31682833›Full record

ReviewJournal of molecular biology2020

Telomere and Subtelomere R-loops and Antigenic Variation in Trypanosomes.

Arpita Saha, Vishal P Nanavaty, Bibo Li

Abstract readReview
In one paragraph

Review in Journal of molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Microbiology spectrum · 2026
    Article
  2. Identification of an active RNAi pathway inProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The ElusivePathogens (Basel, Switzerland) · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Regulation of Antigenic Variation byPathogens (Basel, Switzerland) · 2021
    Review
  14. Article
  15. Review
  16. Review
  17. Science advances · 2020
    Article
  18. An Evolutionary View ofFrontiers in cellular and infection microbiology · 2019
    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

3 authors.

Arpita SahaCenter for Gene Regulation in Health and Disease, Department of Biological, Geological, and Environmental Sciences, College of Science and Health Professions, Cleveland State University, 2121 Euclid Avenue, Cleveland, OH 44115, USA.
Vishal P NanavatyCenter for Gene Regulation in Health and Disease, Department of Biological, Geological, and Environmental Sciences, College of Science and Health Professions, Cleveland State University, 2121 Euclid Avenue, Cleveland, OH 44115, USA.
Bibo LiCenter for Gene Regulation in Health and Disease, Department of Biological, Geological, and Environmental Sciences, College of Science and Health Professions, Cleveland State University, 2121 Euclid Avenue, Cleveland, OH 44115, USA; Case Comprehensive Cancer Center, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA; Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA. Electronic address: b.li37@csuohio.edu.

Funding

Mechanisms of RAP1 functions in monoallelic VSG expression in Trypanosoma bruceiR01AI066095 · NIAID · CLEVELAND STATE UNIVERSITY · PI LI, BIBO · 2007 to 2020
$5.2M
Molecular dynamics of genome and epigenome integrity in Trypanosoma bruceiR01AI127562 · NIAID · ROCKEFELLER UNIVERSITY · PI KIM, HEE-SOOK · 2017 to 2021
$1.7M
A Digital Laser Scanner Biomolecular Imaging System: Amersham Typhoon 5S10OD025252 · OD · CLEVELAND STATE UNIVERSITY · PI LI, BIBO · 2018 to 2018
$163k
NIAID NIH HHS R01 AI066095NIAID NIH HHS R01 AI127562NIH HHS S10 OD025252
6 · The paper itself

Abstract

Trypanosoma brucei is a kinetoplastid parasite that causes African trypanosomiasis, which is fatal if left untreated. T. brucei regularly switches its major surface antigen, VSG, to evade the host immune responses. VSGs are exclusively expressed from subtelomeric expression sites (ESs) where VSG genes are flanked by upstream 70 bp repeats and downstream telomeric repeats. The telomere downstream of the active VSG is transcribed into a long-noncoding RNA (TERRA), which forms RNA:DNA hybrids (R-loops) with the telomeric DNA. At an elevated level, telomere R-loops cause more telomeric and subtelomeric double-strand breaks (DSBs) and increase VSG switching rate. In addition, stabilized R-loops are observed at the 70 bp repeats and immediately downstream of ES-linked VSGs in RNase H defective cells, which also have an increased amount of subtelomeric DSBs and more frequent VSG switching. Although subtelomere plasticity is expected to be beneficial to antigenic variation, severe defects in subtelomere integrity and stability increase cell lethality. Therefore, regulation of the telomere and 70 bp repeat R-loop levels is important for the balance between antigenic variation and cell fitness in T. brucei. In addition, the high level of the active ES transcription favors accumulation of R-loops at the telomere and 70 bp repeats, providing an intrinsic mechanism for local DSB formation, which is a strong inducer of VSG switching.

Indexed as

Antigenic VariationCell PlasticityGenetic VariationR-Loop StructuresRNA, TransferTelomereTrypanosoma brucei bruceiVariant Surface Glycoproteins, TrypanosomaRNA, TransferVariant Surface Glycoproteins, Trypanosoma70 bp repeatsAntigenic variationR-loopTelomereTERRA

Identifiers

PMID31682833
PMCPMC7195242

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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.