Evidence map›Paper›PMID 23812681›Full record

ArticleThe Journal of antimicrobial chemotherapy2013

Trans-translation mediates tolerance to multiple antibiotics and stresses in Escherichia coli.

Jinghua Li, Lei Ji, Wanliang Shi, Jianping Xie, Ying Zhang

Open access · greenAbstract read
In one paragraph

Article in The Journal of antimicrobial chemotherapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 20% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Cooperative and Independent Functionality of tmRNA and SmpB inInternational journal of molecular sciences · 2025
    Article
  6. Article
  7. Article
  8. Bacterial persisters: molecular mechanisms and therapeutic development.Signal transduction and targeted therapy · 2024
    Review
  9. Convergent genetic adaptation ofFrontiers in molecular biosciences · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Infection and drug resistance · 2023
    Article
  14. Article
  15. PurN Is Involved in Antibiotic Tolerance and Virulence inAntibiotics (Basel, Switzerland) · 2022
    Article
  16. Article
  17. Peptide Aptamer PA3 Attenuates the Viability ofFrontiers in microbiology · 2022
    Article
  18. Article
  19. Microorganisms · 2021
    Review
  20. IreK-Mediated, Cell Wall-Protective Phosphorylation inJournal of proteome research · 2021
    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 3 institutions in 2 countries.

Jinghua LiDepartment of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Lei Ji
Wanliang Shi
Jianping Xie
Ying Zhang
Johns Hopkins University · USSouthwest University · CNFirst Bethune Hospital of Jilin University · CN

Funding

Pyrazinamide and Trans-Translation in Mycobacterium tuberculosisR01AI099512 · NIAID · JOHNS HOPKINS UNIVERSITY · PI ZHANG, YING · 2012 to 2015
$1.7M
NIAID NIH HHS AI099512NIAID NIH HHS R01 AI099512
6 · The paper itself

Abstract

backgroundTrans-translation mediated by SsrA (tmRNA) and its associated protein SmpB plays an important role in rescuing stalled ribosomes and detoxifying toxic protein products under stress conditions. However, the role of SsrA and SmpB in bacterial persister survival has not been studied. The recent finding that pyrazinamide as a unique persister drug inhibits trans-translation in Mycobacterium tuberculosis prompted us to examine the role of trans-translation in persister survival.

methodsUsing Escherichia coli as a model, we constructed SsrA and SmpB mutants and assessed the susceptibility of the mutants to various antibiotics and stress conditions in MIC/MBC and persister assays.

resultsWe found that mutations in SsrA and SmpB caused a defect in persister survival as shown by their increased susceptibility to a variety of antibiotics, including gentamicin, streptomycin, amikacin, norfloxacin, trimethoprim and tetracycline, and also stresses, such as acid, weak acid salicylate, heat and peroxide. Additionally, the SsrA and SmpB mutants were 2-8-fold more susceptible than the parent strain to various antibiotics in MIC and MBC tests. The SmpB mutant was more susceptible to antibiotics and stresses than the SsrA mutant. A particularly interesting finding is the hypersusceptibility of the SmpB mutant and the SsrA mutant to trimethoprim. The defect of various SsrA and SmpB mutant phenotypes could be complemented by functional ssrA and smpB, respectively.

conclusionsWe conclude that SsrA and SmpB are important for persister survival and may serve as a good target for developing new antibiotics that kill persister bacteria for improved treatment of persistent bacterial infections.

Indexed as

Drug ToleranceProtein BiosynthesisStress, PhysiologicalAcidsAnti-Bacterial AgentsEscherichia coliGene DeletionHot TemperatureHumansMicrobial Sensitivity TestsMicrobial ViabilityOxidantsRNA-Binding ProteinsAcidsAnti-Bacterial AgentsOxidantsRNA-Binding Proteinssmall protein Bdrug targetdrug tolerancepersistencepersister mechanismspersisters

Identifiers

PMID23812681
PMCPMC3797643
OpenAlexW2103334265

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.