Evidence map›Paper›PMID 16547055›Full record

ArticleJournal of bacteriology2006

Molecular and physiological effects of mycobacterial oxyR inactivation.

Eileen Pagán-Ramos, Sharon S Master, Christopher L Pritchett, Renate Reimschuessel, Michele Trucksis, Graham S Timmins, Vojo Deretic

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Growth in biofilms preparesFrontiers in microbiology · 2025
    Article
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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

7 authors at 5 institutions in 1 country.

Eileen Pagán-RamosDepartment of Microbiology, University of Michigan Medical School, Ann Arbor, Michigan 48105, USA.
Sharon S Master
Christopher L Pritchett
Renate Reimschuessel
Michele Trucksis
Graham S Timmins
Vojo Deretic
Center for Veterinary Medicine · USUniversity of Maryland, Baltimore · USUniversity of Massachusetts Chan Medical School · USUniversity of Michigan–Ann Arbor · USUniversity of New Mexico · US

Funding

Pattern Recognition Receptors and Autophagy in Mtb Control in AIDSR01AI042999 · NIAID · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI DERETIC, VOJO P · 1998 to 2017
$6.6M
Pattern Recognition Receptors and Autophagy in Mtb Control in AIDSR37AI042999 · NIAID · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI VOJO P DERETIC · 2018 to 2026
$4.7M
Antimycobacterial NO from KatG Activation of IsoniazidR21AI063486 · NIAID · UNIVERSITY OF NEW MEXICO · PI TIMMINS, GRAHAM S · 2006 to 2007
$370k
NIAID NIH HHS AI063486NIAID NIH HHS AI42999NIAID NIH HHS R01 AI042999NIAID NIH HHS R21 AI063486NIAID NIH HHS R37 AI042999
6 · The paper itself

Abstract

The majority of slow-growing mycobacteria have a functional oxyR, the central regulator of the bacterial oxidative stress response. In contrast, this gene has been inactivated during the evolution of Mycobacterium tuberculosis. Here we inactivated the oxyR gene in Mycobacterium marinum, an organism used to model M. tuberculosis pathogenesis. Inactivation of oxyR abrogated induction of ahpC, a gene encoding alkylhydroperoxide reductase, normally activated upon peroxide challenge. The absence of oxyR also resulted in increased sensitivity to the front-line antituberculosis drug isoniazid. Inactivation of oxyR in M. marinum did not affect either virulence in a fish infection model or survival in human macrophages. Our findings demonstrate, at the genetic and molecular levels, a direct role for OxyR in ahpC regulation in response to oxidative stress. Our study also indicates that oxyR is not critical for virulence in M. marinum. However, oxyR inactivation confers increased sensitivity to isonicotinic acid hydrazide, suggesting that the natural loss of oxyR in the tubercle bacillus contributes to the unusually high sensitivity of M. tuberculosis to isoniazid.

Indexed as

AnimalsAntitubercular AgentsBacterial ProteinsDNA-Binding ProteinsDrug Resistance, BacterialFish DiseasesGene DeletionGoldfishIsoniazidMycobacterium marinumOxidative StressPeroxidesRepressor ProteinsTranscription FactorsAntitubercular AgentsBacterial ProteinsDNA-Binding ProteinsIsoniazidPeroxidesRepressor ProteinsTranscription Factors

Identifiers

PMID16547055
PMCPMC1428386
OpenAlexW2128794106

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.