Evidence map›Paper›PMID 19997622›Full record

ArticlePLoS pathogens2009

Central role of the Holliday junction helicase RuvAB in vlsE recombination and infectivity of Borrelia burgdorferi.

Tao Lin, Lihui Gao, Diane G Edmondson, Mary B Jacobs, Mario T Philipp, Steven J Norris

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

54 citing papers in PubMed, 82 citations in OpenAlex.

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  10. Lyme Disease Pathogenesis.Current issues in molecular biology · 2021
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  13. Complement Evasion inAntibiotics (Basel, Switzerland) · 2019
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  14. Review
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  18. Article
  19. Article
  20. Antigenic Variation in Bacterial Pathogens.Microbiology spectrum · 2016
    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

6 authors at 2 institutions in 1 country.

Tao LinDepartment of Pathology and Laboratory Medicine, Medical School, University of Texas Health Science Center at Houston, Texas, United States of America.
Lihui Gao
Diane G Edmondson
Mary B Jacobs
Mario T Philipp
Steven J Norris
The University of Texas Health Science Center at Houston · USTulane University · US

Funding

VIRULENCE-ASSOCIATED PROTEINS IN LYME DISEASER01AI037277 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI NORRIS, STEVEN J. · 1995 to 2015
$5.4M
Virulence Determinants of Borrelia burgdorferiR01AI059048 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI NORRIS, STEVEN J. · 2004 to 2016
$5.3M
NIAID NIH HHS R01 AI037277NIAID NIH HHS R01 AI059048NIAID NIH HHS R01AI059048NIAID NIH HHS R01AI37277
6 · The paper itself

Abstract

Antigenic variation plays a vital role in the pathogenesis of many infectious bacteria and protozoa including Borrelia burgdorferi, the causative agent of Lyme disease. VlsE, a 35 kDa surface-exposed lipoprotein, undergoes antigenic variation during B. burgdorferi infection of mammalian hosts, and is believed to be a critical mechanism by which the spirochetes evade immune clearance. Random, segmental recombination between the expressed vlsE gene and adjacent vls silent cassettes generates a large number of different VlsE variants within the infected host. Although the occurrence and importance of vlsE sequence variation is well established, little is known about the biological mechanism of vlsE recombination. To identify factors important in antigenic variation and vlsE recombination, we screened transposon mutants of genes known to be involved in DNA recombination and repair for their effects on infectivity and vlsE recombination. Several mutants, including those in BB0023 (ruvA), BB0022 (ruvB), BB0797 (mutS), and BB0098 (mutS-II), showed reduced infectivity in immunocompetent C3H/HeN mice. Mutants in ruvA and ruvB exhibited greatly reduced rates of vlsE recombination in C3H/HeN mice, as determined by restriction fragment polymorphism (RFLP) screening and DNA sequence analysis. In severe combined immunodeficiency (C3H/scid) mice, the ruvA mutant retained full infectivity; however, all recovered clones retained the 'parental' vlsE sequence, consistent with low rates of vlsE recombination. These results suggest that the reduced infectivity of ruvA and ruvB mutants is the result of ineffective vlsE recombination and underscores the important role that vlsE recombination plays in immune evasion. Based on functional studies in other organisms, the RuvAB complex of B. burgdorferi may promote branch migration of Holliday junctions during vlsE recombination. Our findings are consistent with those in the accompanying article by Dresser et al., and together these studies provide the first examples of trans-acting factors involved in vlsE recombination.

Indexed as

Recombination, GeneticAnimalsAntigens, BacterialBacterial ProteinsBorrelia burgdorferiCluster AnalysisDNA DamageDNA HelicasesDNA RepairDNA Transposable ElementsGenetic Complementation TestIxodesLipoproteinsMiceMice, SCIDMutationAntigens, BacterialBacterial ProteinsDNA HelicasesDNA Transposable ElementsLipoproteinsRuvB protein, BacteriaVlsE protein, Borrelia burgdorferi

Identifiers

PMID19997622
PMCPMC2780311
OpenAlexW1970411207

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.