Evidence map›Paper›PMID 24363348›Full record

ArticleJournal of bacteriology2014

The LuxR-type regulator VpsT negatively controls the transcription of rpoS, encoding the general stress response regulator, in Vibrio cholerae biofilms.

Hongxia Wang, Julio C Ayala, Jorge A Benitez, Anisia J Silva

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bacteriology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. A putative siderophore receptor ofFrontiers in microbiology · 2022
    Article
  6. Article
  7. Motility of Vibrio spp.: regulation and controlling strategies.Applied microbiology and biotechnology · 2020
    Review
  8. Transcription Factor Analysis in Trypanosomatids.Methods in molecular biology (Clifton, N.J.) · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Vibrio cholerae Biofilms and Cholera Pathogenesis.PLoS neglected tropical diseases · 2016
    Review
  19. Review
  20. Identification and Characterization of anFrontiers in microbiology · 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

4 authors at 3 institutions in 1 country.

Hongxia WangMorehouse School of Medicine, Department of Microbiology, Biochemistry and Immunology, Atlanta, Georgia, USA.
Julio C Ayala
Jorge A Benitez
Anisia J Silva
Morehouse School of Medicine · USSouthern Research Institute · USUniversity of Alabama at Birmingham · US

Funding

Morehouse School of Medicine Center of Excellence Research Endowment ProgramS21MD000101 · NIMHD · MOREHOUSE SCHOOL OF MEDICINE · PI MONTGOMERY-RICE, VALERIE C. · 2001 to 2015
$74.3M
Regulation of Vibrio cholerae motility, stress response and detachment from intesSC1AI104993 · NIAID · MOREHOUSE SCHOOL OF MEDICINE · PI SILVA-BENITEZ, ANISIA J · 2012 to 2015
$1.3M
Regulation of Vibrio Biofilm Formation by H-NS Repression and Anti-repression.F31AI106288 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AYALA, JULIO CESAR · 2014 to 2016
$99k
NIAID NIH HHS AI104993-02NIAID NIH HHS F31 AI106288NIAID NIH HHS SC1 AI104993NIMHD NIH HHS S21 MD000101
6 · The paper itself

Abstract

Cholera is a waterborne diarrheal disease caused by Vibrio cholerae strains of serogroups O1 and O139. Expression of the general stress response regulator RpoS and formation of biofilm communities enhance the capacity of V. cholerae to persist in aquatic environments. The transition of V. cholerae between free-swimming (planktonic) and biofilm life-styles is regulated by the second messenger cyclic di-GMP (c-di-GMP). We previously reported that increasing the c-di-GMP pool by overexpression of a diguanylate cyclase diminished RpoS expression. Here we show that c-di-GMP repression of RpoS expression is eliminated by deletion of the genes vpsR and vpsT, encoding positive regulators of biofilm development. To determine the mechanism of this regulation, we constructed a strain expressing a vpsT-FLAG allele from native transcription and translation signals. Increasing the c-di-GMP pool induced vpsT-FLAG expression. The interaction between VpsT-FLAG and the rpoS promoter was demonstrated by chromatin immunoprecipitation. Furthermore, purified VpsT interacted with the rpoS promoter in a c-di-GMP-dependent manner. Primer extension analysis identified two rpoS transcription initiation sites located 43 bp (P1) and 63 bp (P2) upstream of the rpoS start codon. DNase I footprinting showed that the VpsT binding site at the rpoS promoter overlaps the primary P1 transcriptional start site. Deletion of vpsT significantly enhanced rpoS expression in V. cholerae biofilms that do not make HapR. This result suggests that VpsT and c-di-GMP contribute to the transcriptional silencing of rpoS in biofilms prior to cells entering the quorum-sensing mode.

Indexed as

Bacterial ProteinsBiofilmsCyclic GMPGene Expression Regulation, BacterialSigma FactorStress, PhysiologicalTranscription, GeneticVibrio choleraeBacterial Proteinsbis(3',5')-cyclic diguanylic acidCyclic GMPSigma Factorsigma factor KatF protein, Bacteria

Identifiers

PMID24363348
PMCPMC3957697
OpenAlexW2109911082

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.