Evidence map›Paper›PMID 22514651›Full record

ArticlePloS one2012

DotU and VgrG, core components of type VI secretion systems, are essential for Francisella LVS pathogenicity.

Jeanette E Bröms, Lena Meyer, Moa Lavander, Pär Larsson, Anders Sjöstedt

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
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  5. Type VI secretion systems promote intraspecific competition and host interactions in a bee gut symbiont.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Review
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  15. Article
  16. Article
  17. Article
  18. Frontiers in microbiology · 2018
    Article
  19. Article
  20. Differential Growth ofFrontiers in microbiology · 2017
    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.

Jeanette E BrömsClinical Bacteriology, Department of Clinical Microbiology, and Laboratory for Molecular Infection Medicine Sweden, Umeå University, Umeå, Sweden. jeanette.broms@climi.umu.se
Lena Meyer
Moa Lavander
Pär Larsson
Anders Sjöstedt
Umeå University · SESwedish Defence Research Agency · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Gram-negative bacterium Francisella tularensis causes tularemia, a disease which requires bacterial escape from phagosomes of infected macrophages. Once in the cytosol, the bacterium rapidly multiplies, inhibits activation of the inflammasome and ultimately causes death of the host cell. Of importance for these processes is a 33-kb gene cluster, the Francisella pathogenicity island (FPI), which is believed to encode a type VI secretion system (T6SS). In this study, we analyzed the role of the FPI-encoded proteins VgrG and DotU, which are conserved components of type VI secretion (T6S) clusters. We demonstrate that in F. tularensis LVS, VgrG was shown to form multimers, consistent with its suggested role as a trimeric membrane puncturing device in T6SSs, while the inner membrane protein DotU was shown to stabilize PdpB/IcmF, another T6SS core component. Upon infection of J774 cells, both ΔvgrG and ΔdotU mutants did not escape from phagosomes, and subsequently, did not multiply or cause cytopathogenicity. They also showed impaired activation of the inflammasome and marked attenuation in the mouse model. Moreover, all of the DotU-dependent functions investigated here required the presence of three residues that are essentially conserved among all DotU homologues. Thus, in agreement with a core function in T6S clusters, VgrG and DotU play key roles for modulation of the intracellular host response as well as for the virulence of F. tularensis.

Indexed as

Bacterial ProteinsFrancisellaGenomic IslandsTumor Necrosis Factor-alphaBacterial ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID22514651
PMCPMC3326028
OpenAlexW2071708833

What OpenQuestion holds

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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.