Evidence map›Paper›PMID 21821774›Full record

ArticleJournal of bacteriology2011

Components of the Rv0081-Rv0088 locus, which encodes a predicted formate hydrogenlyase complex, are coregulated by Rv0081, MprA, and DosR in Mycobacterium tuberculosis.

Hongjun He, Daniel J Bretl, Renee M Penoske, David M Anderson, Thomas C Zahrt

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. A Systematic Review on NovelFrontiers in immunology · 2018
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. DosR's multifaceted role onFrontiers in cellular and infection microbiology · 2023
    Article
  10. Potential therapeutic approaches for a sleeping pathogen: tuberculosis a case for bioinorganic chemistry.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2020
    Review
  11. Review
  12. The sensor kinase MtrB ofThe Journal of biological chemistry · 2019
    Article
  13. MTS1338, A SmallFrontiers in cellular and infection microbiology · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Hongjun HeDepartment of Microbiology and Molecular Genetics, Center for Infectious Disease Research, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226-0509, USA.
Daniel J Bretl
Renee M Penoske
David M Anderson
Thomas C Zahrt
Medical College of Wisconsin · US

Funding

M.tuberculosis Genes Regulating Persistent InfectionR01AI051669 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI ZAHRT, THOMAS C. · 2001 to 2011
$3.5M
NIAID NIH HHS R01 AI051669NIAID NIH HHS R01 AI51669
6 · The paper itself

Abstract

Mycobacterium tuberculosis, the etiological agent of tuberculosis, remains a significant cause of morbidity and mortality throughout the world despite a vaccine and cost-effective antibiotics. The success of this organism can be attributed, in part, to its ability to adapt to potentially harmful stress within the host and establish, maintain, and reactivate from long-term persistent infection within granulomatous structures. The DosRS-DosT/DevRS-Rv2027c, and MprAB two-component signal transduction systems have previously been implicated in aspects of persistent infection by M. tuberculosis and are known to be responsive to conditions likely to be found within the granuloma. Here, we describe initial characterization of a locus (Rv0081-Rv0088) encoding components of a predicted formate hydrogenylase enzyme complex that is directly regulated by DosR/DevR and MprA, and the product of the first gene in this operon, Rv0081. In particular, we demonstrate that Rv0081 negatively regulates its own expression and that of downstream genes by binding an inverted repeat element in its upstream region. In contrast, DosR/DevR and MprA positively regulate Rv0081 expression by binding to recognition sequences that either partially or completely overlap that recognized by Rv0081, respectively. Expression of Rv0081 initiates from two promoter elements; one promoter located downstream of the DosR/DevR binding site but overlapping the sequence recognized by both Rv0081 and MprA and another promoter downstream of the DosR/DevR, Rv0081, and MprA binding sites. Interestingly, Rv0081 represses Rv0081 and downstream determinants following activation of DosRS-DosT/DevRS-Rv2027c by nitric oxide, suggesting that expression of this locus is complex and subject to multiple levels of regulation. Based on this and other published information, a model is proposed detailing Rv0081-Rv0088 expression by these transcription factors within particular growth environments.

Indexed as

Bacterial ProteinsDNA-Binding ProteinsElectrophoretic Mobility Shift AssayFormate DehydrogenasesGene Expression Regulation, BacterialMultienzyme ComplexesMutationMycobacterium tuberculosisProtamine KinaseProtein KinasesReverse Transcriptase Polymerase Chain ReactionBacterial ProteinsDevS protein, Mycobacterium tuberculosisDNA-Binding ProteinsDosR protein, Mycobacterium tuberculosisFormate DehydrogenasesMprA protein, Mycobacterium tuberculosisMultienzyme ComplexesProtamine KinaseProtein Kinases

Identifiers

PMID21821774
PMCPMC3187382
OpenAlexW1990317495

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.