Evidence map›Paper›PMID 15901695›Full record

ArticleJournal of bacteriology2005

Regulation of mtrF expression in Neisseria gonorrhoeae and its role in high-level antimicrobial resistance.

Jason P Folster, William M Shafer

Abstract read
In one paragraph

Article in Journal of bacteriology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 16% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. MarR family proteins are important regulators of clinically relevant antibiotic resistance.Protein science : a publication of the Protein Society · 2020
    Review
  6. Article
  7. Structural, Biochemical, andJournal of bacteriology · 2019
    Article
  8. Bacterial Adaptation to Antibiotics through Regulatory RNAs.Antimicrobial agents and chemotherapy · 2018
    Review
  9. Control ofmBio · 2017
    Article
  10. Article
  11. The AbgT family: A novel class of antimetabolite transporters.Protein science : a publication of the Protein Society · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Jason P FolsterDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
William M Shafer
Emory University · USVeterans Health Administration · US

Funding

GONOCOCCI: GENETICS OF RESISTANCE TO PMN PROTEINSR01AI021150 · NIAID · EMORY UNIVERSITY · PI SHAFER, WILLIAM MAURICE · 1985 to 2025
$5.5M
Gonococci: Genetics of Resistance to PMN ProteinsR37AI021150 · NIAID · EMORY UNIVERSITY · PI SHAFER, WILLIAM MAURICE · 2010 to 2019
$3.9M
MOLECULAR MECHANISMS OF MICROBIAL PATHOGENESIST32AI007470 · NIAID · EMORY UNIVERSITY · PI SPECK, SAMUEL H · 1995 to 2010
$3.2M
MICROBIAL PATHOGEN GENOME PROJECT--NEISSERIA GONORRHOEAER01AI038399 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI DYER, DAVID W. · 1995 to 1998
–
NIAID NIH HHS 5T32 AI-07470NIAID NIH HHS AI-21150-19NIAID NIH HHS AI-38399NIAID NIH HHS R01 AI021150NIAID NIH HHS R37 AI021150NIAID NIH HHS T32 AI007470
6 · The paper itself

Abstract

The obligate human pathogen Neisseria gonorrhoeae uses the MtrC-MtrD-MtrE efflux pump to resist structurally diverse hydrophobic antimicrobial agents (HAs), some of which bathe mucosal surfaces that become infected during transmission of gonococci. Constitutive high-level HA resistance occurs by the loss of a repressor (MtrR) that negatively controls transcription of the mtrCDE operon. This high-level HA resistance also requires the product of the mtrF gene, which is located downstream and transcriptionally divergent from mtrCDE. MtrF is a putative inner membrane protein, but its role in HA resistance mediated by the MtrC-MtrD-MtrE efflux pump remains to be determined. High-level HA resistance can also be mediated through an induction process that requires enhanced transcription of mtrCDE when gonococci are grown in the presence of a sublethal concentration of Triton X-100. We now report that inactivation of mtrF results in a significant reduction in the induction of HA resistance and that the expression of mtrF is enhanced when gonococci are grown under inducing conditions. However, no effect was observed on the induction of mtrCDE expression in an MtrF-negative strain. The expression of mtrF was repressed by MtrR, the major repressor of mtrCDE expression. In addition to MtrR, another repressor (MpeR) can downregulate the expression of mtrF. Repression of mtrF by MtrR and MpeR was additive, demonstrating that the repressive effects mediated by these regulators are independent processes.

Indexed as

Amino Acid SequenceBacterial Outer Membrane ProteinsBacterial ProteinsConsensus SequenceDrug Resistance, BacterialGene Expression Regulation, BacterialLipoproteinsMembrane ProteinsMembrane Transport ProteinsMolecular Sequence DataNeisseria gonorrhoeaeRepressor ProteinsTranscriptional ActivationBacterial Outer Membrane ProteinsBacterial ProteinsLipoproteinsMembrane ProteinsMembrane Transport ProteinsMtrC protein, Neisseria gonorrhoeaeMtrD protein, Neisseria gonorrhoeaeMtrE protein, Neisseria gonorrhoeaemtrR protein, Neisseria gonorrhoeaeRepressor Proteins

Identifiers

PMID15901695
PMCPMC1112036
OpenAlexW1988972551

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.