Evidence map›Paper›PMID 26502963›Full record

ArticleJournal of microbiology (Seoul, Korea)2015

The Mycobacterium tuberculosis relBE toxin:antitoxin genes are stress-responsive modules that regulate growth through translation inhibition.

Shaleen B Korch, Vandana Malhotra, Heidi Contreras, Josephine E Clark-Curtiss

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Journal of microbiology (Seoul, Korea), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
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

29 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Enhancement of mycobacterial pathogenesis by host interferon-γ.Cellular and molecular life sciences : CMLS · 2024
    Article
  9. Bacterial persisters: molecular mechanisms and therapeutic development.Signal transduction and targeted therapy · 2024
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Comparative Genomic Analysis of the Human PathogenFrontiers in cellular and infection microbiology · 2022
    Article
  16. Review
  17. Article
  18. Mobilome Analysis ofMicroorganisms · 2021
    Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Shaleen B KorchCenter for Infectious Diseases and Vaccinology, Biodesign Institute, Arizona State University, Tempe, Arizona, 85287, USA. skorch@midwestern.edu.
Vandana MalhotraCenter for Infectious Diseases and Vaccinology, Biodesign Institute, Arizona State University, Tempe, Arizona, 85287, USA.
Heidi ContrerasCenter for Infectious Diseases and Vaccinology, Biodesign Institute, Arizona State University, Tempe, Arizona, 85287, USA.
Josephine E Clark-CurtissCenter for Infectious Diseases and Vaccinology, Biodesign Institute, Arizona State University, Tempe, Arizona, 85287, USA.
Arizona State University · USMidwestern University · USUniversity of California, Irvine · US

Funding

GENE EXPRESSION IN MYCOBACTERIUM TUBERCULOSISR01AI046428 · NIAID · WASHINGTON UNIVERSITY · PI CLARK-CURTISS, JOSEPHINE E · 2000 to 2009
$2.6M
Arizona State University PREP for Biomedical ResearchR25GM071798 · NIGMS · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI HOGUE, BRENDA G. · 2004 to 2014
$2.4M
NIAID NIH HHS AI46428NIAID NIH HHS R01 AI046428NIGMS NIH HHS GM071798NIGMS NIH HHS R25 GM071798
6 · The paper itself

Abstract

Toxin-antitoxin (TA) genes are ubiquitous among bacteria and are associated with persistence and dormancy. Following exposure to unfavorable environmental stimuli, several species (Escherichia coli, Staphylococcus aureus, Myxococcus xanthus) employ toxin proteins such as RelE and MazF to downregulate growth or initiate cell death. Mycobacterium tuberculosis possesses three Rel TA modules (Rel Mtb ): RelBE Mtb , RelFG Mtb and RelJK Mtb (Rv1246c-Rv1247c, Rv2865-Rv2866, and Rv3357-Rv3358, respectively), which inhibit mycobacterial growth when the toxin gene (relE, relG, relK) is expressed independently of the antitoxin gene (relB, relF, relJ). In the present study, we examined the in vivo mechanism of the RelE Mtb toxin protein, the impact of RelE Mtb on M. tuberculosis physiology and the environmental conditions that regulate all three rel Mtb modules. RelE Mtb negatively impacts growth and the structural integrity of the mycobacterial envelope, generating cells with aberrant forms that are prone to extensive aggregation. At a time coincident with growth defects, RelE Mtb mediates mRNA degradation in vivo resulting in significant changes to the proteome. We establish that rel Mtb modules are stress responsive, as all three operons are transcriptionally activated following mycobacterial exposure to oxidative stress or nitrogen-limiting growth environments. Here we present evidence that the rel Mtb toxin:antitoxin family is stress-responsive and, through the degradation of mRNA, the RelE Mtb toxin influences the growth, proteome and morphology of mycobacterial cells.

Indexed as

Protein BiosynthesisAntitoxinsBacterial ProteinsBacterial ToxinsGene Expression Regulation, BacterialMycobacterium tuberculosisOperonPhenotypeProteomeRNA, MessengerStress, PhysiologicalAntitoxinsBacterial ProteinsBacterial ToxinsProteomeRNA, MessengergrowthmRNAMycobacterium tuberculosisrelBEstresstoxin:antitoxin

Identifiers

PMID26502963
PMCPMC6426445
OpenAlexW4248120405

What OpenQuestion holds

Textmetadata
LicenceTDM
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.