Evidence map›Paper›PMID 42549574›Full record

ArticleNucleic acids research2026

MiaA-mediated tRNA modifications couple tryptophan attenuation and changes in tRNA abundance to complex phenotypes in Pseudomonas aeruginosa.

Yannick N Frommeyer, Janne G Thöming, Nicolas O Gomez, Svenja Grobe, Matthias Preusse, Alejandro Arce-Rodríguez, Kerstin Neubauer, Benedikt Kennepohl, Tim Kirk, Raimo Franke and 7 more

Abstract read
In one paragraph

Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Yannick N FrommeyerInstitute for Molecular Bacteriology, TWINCORE GmbH, Center of Clinical and Experimental Infection Research, a joint venture of the Hannover Medical School and the Helmholtz Center for Infection Research, Hannover 30625, Germany.ORCID 0009-0001-2485-3724
Janne G ThömingInstitute for Molecular Bacteriology, TWINCORE GmbH, Center of Clinical and Experimental Infection Research, a joint venture of the Hannover Medical School and the Helmholtz Center for Infection Research, Hannover 30625, Germany.ORCID 0000-0002-4415-105X
Nicolas O GomezDepartment of Molecular Bacteriology, Helmholtz Center for Infection Research, Braunschweig 38124, Germany.ORCID 0000-0001-5723-886X
Svenja GrobeInstitute for Molecular Bacteriology, TWINCORE GmbH, Center of Clinical and Experimental Infection Research, a joint venture of the Hannover Medical School and the Helmholtz Center for Infection Research, Hannover 30625, Germany.
Matthias PreusseDepartment of Molecular Bacteriology, Helmholtz Center for Infection Research, Braunschweig 38124, Germany.
Alejandro Arce-RodríguezDepartment of Molecular Bacteriology, Helmholtz Center for Infection Research, Braunschweig 38124, Germany.ORCID 0000-0002-2486-401X
Kerstin NeubauerDepartment of Molecular Bacteriology, Helmholtz Center for Infection Research, Braunschweig 38124, Germany.ORCID 0009-0000-6633-9187
Benedikt KennepohlInstitute for Molecular Bacteriology, TWINCORE GmbH, Center of Clinical and Experimental Infection Research, a joint venture of the Hannover Medical School and the Helmholtz Center for Infection Research, Hannover 30625, Germany.
Tim KirkInstitute for Molecular Bacteriology, TWINCORE GmbH, Center of Clinical and Experimental Infection Research, a joint venture of the Hannover Medical School and the Helmholtz Center for Infection Research, Hannover 30625, Germany.ORCID 0009-0009-0127-5501
Raimo FrankeDepartment of Chemical Biology, Helmholtz Centre for Infection Research, and German Center for Infection Research (DZIF), Partner Site Hannover-Braunschweig, Braunschweig 38124, Germany.ORCID 0000-0002-5407-5521
Mark BrönstrupDepartment of Chemical Biology, Helmholtz Centre for Infection Research, and German Center for Infection Research (DZIF), Partner Site Hannover-Braunschweig, Braunschweig 38124, Germany.
Meina Neumann-SchaalDepartment of Metabolomics & Services, Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures, Braunschweig 38124, Germany.ORCID 0000-0002-1641-019X
Mathias MüskenCentral Facility for Microscopy, Helmholtz Centre for Infection Research, Braunschweig 38124, Germany.
Daniel P DepledgeInstitute of Virology, Hanover Medical School, Hannover 30625, Germany.ORCID 0000-0002-4292-0599
Heike BähreResearch Core Unit Metabolomics and Institute of Pharmacology, Hannover Medical School, Hannover 30625, Germany.
Andreas PichResearch Core Unit Proteomics and Institute for Toxicology, Hannover Medical School, Hannover 30625, Germany.
Susanne HäusslerInstitute for Molecular Bacteriology, TWINCORE GmbH, Center of Clinical and Experimental Infection Research, a joint venture of the Hannover Medical School and the Helmholtz Center for Infection Research, Hannover 30625, Germany.ORCID 0000-0001-6141-9102

Funding

Deutsche ForschungsgemeinschaftGermany's Excellence Strategy 390874280Ministry of Science and Culture of Lower SaxonyNiedersächsisches Ministerium für Wissenschaft und KulturNNF 18OC0033946Novo Nordisk Foundation 18OC0033946
6 · The paper itself

Abstract

Transfer RNA (tRNA)-modifying enzymes are emerging as key regulators of bacterial physiology. MiaA, a tRNA isopentenyltransferase, is well studied in model organisms, but its role in the opportunistic pathogen Pseudomonas aeruginosa remains unclear. Using LC-MS, nanopore tRNA sequencing, as well as transcriptional, translational, and proteomic profiling, we mapped MiaA-dependent tRNA modifications and revealed unexpected effects of MiaA loss. Impaired translation of MiaA-sensitive codons reduced quorum-sensing-controlled virulence gene expression and attenuated pathogenicity in Galleria mellonella. Ribosome stalling at trp codons in miaA mutants overrides the attenuation-controlled repression of tryptophan biosynthesis, causing overproduction of tryptophan, along with upregulation of cognate tRNAs, thereby linking translation to global metabolic adaptation. MiaA is tightly regulated and is so central to bacterial physiology that its expression level correlates directly to virulence in clinical isolates, highlighting its role as a hub connecting translation, transcription, metabolism, and pathogenicity. These findings position MiaA as a key integrator of cellular processes critical for pathogen fitness and host interactions.

Indexed as

Bacterial ProteinsPseudomonas aeruginosaRNA Processing, Post-TranscriptionalRNA, TransferTryptophanAnimalsGene Expression Regulation, BacterialPhenotypeProtein BiosynthesisQuorum SensingVirulenceBacterial ProteinsRNA, TransferTryptophan

Identifiers

PMID42549574
PMCPMC13434334

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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.