Evidence map›Paper›PMID 21602215›Full record

ArticleMicrobiology (Reading, England)2011

Helicobacter pylori perceives the quorum-sensing molecule AI-2 as a chemorepellent via the chemoreceptor TlpB.

Bethany A Rader, Christopher Wreden, Kevin G Hicks, Emily Goers Sweeney, Karen M Ottemann, Karen Guillemin

Open access · greenAbstract read
In one paragraph

Article in Microbiology (Reading, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
6.5field-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

72 citing papers in PubMed, 125 citations in OpenAlex.

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  16. Biofilm ofAntibiotics (Basel, Switzerland) · 2023
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  19. Transcriptome Analysis of the Response of MatureAntibiotics (Basel, Switzerland) · 2022
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12 more citing papers are in PubMed but not listed here.

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.

Bethany A RaderInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.
Christopher WredenInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.
Kevin G HicksInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.
Emily Goers SweeneyInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.
Karen M OttemannDepartment of Microbiology and Environmental Toxicology, University of California, Santa Cruz, CA 95064, USA.
Karen GuilleminInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.
University of Oregon · USUniversity of California, Santa Cruz · US

Funding

Roles for Motility in Helicobactor pylori pathogenesisR01AI050000 · NIAID · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI OTTEMANN, KAREN M · 2002 to 2011
$3.6M
Molecular and genetic analysis of the hielcobacter pylori virulence Factor CagAR01DK075667 · NIDDK · UNIVERSITY OF OREGON · PI GUILLEMIN, KAREN J · 2007 to 2010
$1.1M
NIAID NIH HHS R01 AI050000NIDDK NIH HHS R01 DK075667
6 · The paper itself

Abstract

Helicobacter pylori moves in response to environmental chemical cues using a chemotaxis two-component signal-transduction system. Autoinducer-2 (AI-2) is a quorum-sensing signal produced by the LuxS protein that accumulates in the bacterial environment in a density-dependent manner. We showed previously that a H. pylori luxS mutant was defective in motility on soft agar plates. Here we report that deletion of the luxS gene resulted in swimming behaviour with a reduced frequency of stops as compared to the wild-type strain. Stopping frequency was restored to wild-type levels by genetic complementation of the luxS mutation or by addition of synthetic 4,5-dihydroxy-2,3-pentanedione (DPD), which cyclizes to form AI-2. Synthetic DPD also increased the frequency of stops in wild-type H. pylori, similar to the behaviour induced by the known chemorepellent HCl. We found that whereas mutants lacking the chemoreceptor genes tlpA, tlpC or tlpD responded to an exogenous source of synthetic DPD, the chemoreceptor mutant tlpB was non-responsive to a gradient or uniform distribution of the chemical. Furthermore, a double mutant lacking both tlpB and luxS exhibited chemotactic behaviour similar to the tlpB single mutant, whereas a double mutant lacking both tlpB and the chemotransduction gene cheA behaved like a nonchemotactic cheA single mutant, supporting the model that tlpB functions in a signalling pathway downstream of luxS and upstream of cheA. We conclude that H. pylori perceives LuxS-produced AI-2 as a chemorepellent via the chemoreceptor TlpB.

Indexed as

Quorum SensingBacterial ProteinsCarbon-Sulfur LyasesChemotaxisHelicobacter pyloriHomoserineLactonesPentanesSignal Transduction4,5-dihydroxy-2,3-pentanedioneBacterial ProteinsCarbon-Sulfur LyasesHomoserineLactonesLuxS protein, BacteriaN-octanoylhomoserine lactonePentanes

Identifiers

PMID21602215
PMCPMC3352171
OpenAlexW2150725310

What OpenQuestion holds

Textmetadata
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.