Evidence map›Paper›PMID 39708318›Full record

ArticleCell reports2025

Mutations in mexT bypass the stringent response dependency of virulence in Pseudomonas aeruginosa.

Wendy Figueroa, Adrian Cazares, Eleri A Ashworth, Aaron Weimann, Aras Kadioglu, R Andres Floto, Martin Welch

Abstract read
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. 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.

Wendy FigueroaDepartment of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK; Victor Phillip Dahdaleh Heart & Lung Research Institute, Department of Medicine, University of Cambridge, Cambridge, UK. Electronic address: wf255@cam.ac.uk.
Adrian CazaresWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, UK.
Eleri A AshworthDepartment of Clinical Infection, Microbiology & Immunology, University of Liverpool, Liverpool L69 7BE, UK.
Aaron WeimannVictor Phillip Dahdaleh Heart & Lung Research Institute, Department of Medicine, University of Cambridge, Cambridge, UK; Molecular Immunity Unit, University of Cambridge, Department of Medicine, MRC-Laboratory of Molecular Biology, Cambridge, UK.
Aras KadiogluDepartment of Clinical Infection, Microbiology & Immunology, University of Liverpool, Liverpool L69 7BE, UK.
R Andres FlotoVictor Phillip Dahdaleh Heart & Lung Research Institute, Department of Medicine, University of Cambridge, Cambridge, UK; Molecular Immunity Unit, University of Cambridge, Department of Medicine, MRC-Laboratory of Molecular Biology, Cambridge, UK; Cambridge Centre for Lung Infection, Papworth Hospital, Cambridge, UK.
Martin WelchDepartment of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK. Electronic address: mw240@cam.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/M019411/1Wellcome Trust 107032Wellcome Trust 107032AIAWellcome Trust 226602
6 · The paper itself

Abstract

Pseudomonas aeruginosa produces a wealth of virulence factors whose production is controlled via an intricate regulatory systems network. Here, we uncover a major player in the evolution and regulation of virulence that enhances host colonization and antibiotic resistance. By characterizing a collection of mutants lacking the stringent response (SR), a system key for virulence, we show that the loss of the central regulator MexT bypasses absence of the SR, restoring full activation of virulence pathways. Notably, mexT mutations were associated with resistance to aminoglycosides and the last-resort antibiotic, colistin. Analysis of thousands of P. aeruginosa genomes revealed that mexT mutations are widespread in isolates linked to aggressive antibiotic treatment. Furthermore, in vivo experiments in a murine pulmonary model revealed that mexT mutants display a hypervirulent phenotype associated with bacteremia. Altogether, these findings uncover a key regulator that acts as a genetic switch in the regulation of virulence and antimicrobial resistance.

Indexed as

Bacterial ProteinsMutationPseudomonas aeruginosaAnimalsAnti-Bacterial AgentsColistinDrug Resistance, BacterialHumansMicePseudomonas InfectionsVirulenceVirulence FactorsAnti-Bacterial AgentsBacterial ProteinsColistinVirulence Factorsantimicrobial resistanceCP: Microbiologygenetic switchhypervirulenceMexTpathogen evolutionPseudomonas aeruginosaquorum sensingregulatory networkstringent responsetranscriptome

Identifiers

PMID39708318
PMCPMC7618369

What Socratic holds

Textmetadata
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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 Socratic graph.