Evidence map›Paper›PMID 26507235›Full record

ArticlemBio2015

Intrinsic Antimicrobial Resistance Determinants in the Superbug Pseudomonas aeruginosa.

Justine L Murray, Taejoon Kwon, Edward M Marcotte, Marvin Whiteley

Abstract read
In one paragraph

Article in mBio, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
–field-weighted citation impact
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

61 citing papers in PubMed.

  1. The impact of modulator therapy on theProceedings of the National Academy of Sciences of the United States of America · 2026
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  6. Structural and Computational Analysis ofbioRxiv : the preprint server for biology · 2025
    Article
  7. The role of colony morphotype in shaping gene essentiality inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Modern antiseptics against multidrug-resistantFrontiers in microbiology · 2025
    Article
  11. Article
  12. Perturbation-specific transcriptional mapping for unbiased target elucidation of antibiotics.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

4 authors.

Justine L MurrayDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, Texas, USA Center for Infectious Disease, The University of Texas at Austin, Austin, Texas, USA.
Taejoon KwonDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, Texas, USA Institute of Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas, USA Center for Systems and Synthetic Biology, The University of Texas at Austin, Austin, Texas, USA Department of Biomedical Engineering, School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea.
Edward M MarcotteDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, Texas, USA Institute of Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas, USA Center for Systems and Synthetic Biology, The University of Texas at Austin, Austin, Texas, USA.
Marvin WhiteleyDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, Texas, USA Institute of Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas, USA Center for Infectious Disease, The University of Texas at Austin, Austin, Texas, USA mwhiteley@austin.utexas.edu.

Funding

Next-Generation Proteomics: Massively Parallel Single-Molecule Protein IdentificaDP1GM106408 · NIGMS · UNIVERSITY OF TEXAS AT AUSTIN · PI MARCOTTE, EDWARD M · 2012 to 2016
$3.8M
Genetic determinants of bacterial fitness in polymicrobial wound infectionsR21AI107570 · NIAID · UNIVERSITY OF TEXAS AT AUSTIN · PI WHITELEY, MARVIN · 2014 to 2015
$433k
NIAID NIH HHS R21 AI107570NIGMS NIH HHS DP1 GM106408
6 · The paper itself

Abstract

unlabelledAntimicrobial-resistant bacteria pose a serious threat in the clinic. This is particularly true for opportunistic pathogens that possess high intrinsic resistance. Though many studies have focused on understanding the acquisition of bacterial resistance upon exposure to antimicrobials, the mechanisms controlling intrinsic resistance are not well understood. In this study, we subjected the model opportunistic superbug Pseudomonas aeruginosa to 14 antimicrobials under highly controlled conditions and assessed its response using expression- and fitness-based genomic approaches. Our results reveal that gene expression changes and mutant fitness in response to sub-MIC antimicrobials do not correlate on a genomewide scale, indicating that gene expression is not a good predictor of fitness determinants. In general, fewer fitness determinants were identified for antiseptics and disinfectants than for antibiotics. Analysis of gene expression and fitness data together allowed the prediction of antagonistic interactions between antimicrobials and insight into the molecular mechanisms controlling these interactions. IMPORTANCE: Infections involving multidrug-resistant pathogens are difficult to treat because the therapeutic options are limited. These infections impose a significant financial burden on infected patients and on health care systems. Despite years of antimicrobial resistance research, we lack a comprehensive understanding of the intrinsic mechanisms controlling antimicrobial resistance. This work uses two fine-scale genomic approaches to identify genetic loci important for antimicrobial resistance of the opportunistic pathogen Pseudomonas aeruginosa. Our results reveal that antibiotics have more resistance determinants than antiseptics/disinfectants and that gene expression upon exposure to antimicrobials is not a good predictor of these resistance determinants. In addition, we show that when used together, genomewide gene expression and fitness profiling can provide mechanistic insights into multidrug resistance mechanisms.

Indexed as

Drug Resistance, Multiple, BacterialAnti-Bacterial AgentsGene Expression ProfilingMicrobial Sensitivity TestsMutationPseudomonas aeruginosaAnti-Bacterial Agents

Identifiers

PMID26507235
PMCPMC4626858

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.