Evidence map›Paper›PMID 40623067›Full record

ArticlePLoS pathogens2025

Yersinia pseudotuberculosis growth arrest during type-III secretion system expression is associated with altered ribosomal protein expression and decreased gentamicin susceptibility.

Justin Greene, Katherine L Cotten, Rhett A Snyder, Ryan C Huiszoon, Sangwook Chu, Rezia Era D Braza, Ashley A Chapin, Justin M Stine, William E Bentley, Reza Ghodssi and 1 more

Abstract read
In one paragraph

Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Regulator-derived growth and fitness costs ofbioRxiv : the preprint server for biology · 2026
    Article
  3. Article
4 · The record

Corrections and comments

  • Update of
    2024
5 · Who and what money

Authors and funding

11 authors.

Justin GreeneW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America.
Katherine L CottenW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America.
Rhett A SnyderW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America.
Ryan C HuiszoonInstitute for Systems Research, University of Maryland, College Park, Maryland, United States of America.
Sangwook ChuInstitute for Systems Research, University of Maryland, College Park, Maryland, United States of America.
Rezia Era D BrazaW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America.
Ashley A ChapinInstitute for Systems Research, University of Maryland, College Park, Maryland, United States of America.
Justin M StineInstitute for Systems Research, University of Maryland, College Park, Maryland, United States of America.
William E BentleyFischell Department of Bioengineering, University of Maryland, College Park, Maryland, United States of America.
Reza GhodssiInstitute for Systems Research, University of Maryland, College Park, Maryland, United States of America.
Kimberly M DavisW. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America.ORCID 0000-0003-1870-3137

Funding

Medical Scientist Training ProgramT32GM136577 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI ANDREA L COX · 2020 to 2026
$13.4M
Training: Molecular & Cellular Bases of Infectious DiseasesT32AI007417 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Arturo Casadevall · 1994 to 2026
$11.9M
Identifying the pathways associated with bacterial antibiotic persistence within host tissuesR01AI175307 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Kim Davis · 2023 to 2026
$2.3M
Contribution of innate immune cells in promoting antibiotic toleranceR21AI154116 · NIAID · JOHNS HOPKINS UNIVERSITY · PI DAVIS, KIM · 2021 to 2022
$450k
Community behavior of Yersinia pseudotuberculosis within microcoloniesK22AI123465 · NIAID · JOHNS HOPKINS UNIVERSITY · PI DAVIS, KIM · 2017 to 2018
$270k
NIAID NIH HHS K22 AI123465NIAID NIH HHS R01 AI175307NIAID NIH HHS R21 AI154116NIAID NIH HHS T32 AI007417NIGMS NIH HHS T32 GM136577
6 · The paper itself

Abstract

It has been long appreciated that expression of the Yersinia type-III secretion system (T3SS) in culture is associated with growth arrest. Here we sought to understand whether T3SS expression is sufficient to trigger loss of exponential phase markers, and utilized a fluorescent reporter for ribosomal protein expression to detect changes in bacterial growth state. Using a fluorescent transcriptional reporter with the rpsJ/S10 promoter fused to a destabilized gfp variant, we confirmed reporter expression significantly increases in exponential phase and decreases as cells transition to stationary phase. In a mouse model of systemic Y. pseudotuberculosis infection, we found multiple subsets of bacterial cells in the mouse spleen, including cells with high T3SS and low S10 expression and cells with high expression of both markers. In bacterial media, growth inhibition with T3SS induction and a reduction in S10 expression were observed, but a significant proportion of cells retained high expression of both T3SS and S10. Paradoxically, while loss of T3SS expression rescued growth, lower S10 expression was detected, again indicating bacteria can express both markers simultaneously. In media, bacteria grow planktonically as individual cells, while in mouse tissues, bacteria form clustered extracellular communities. We utilized droplet-based microfluidics to encapsulate bacteria in spherical agarose droplets and model clustered growth, and observed high expression of T3SS without an impact on S10 levels. Finally, we show that T3SS expression is sufficient to promote antibiotic tolerance, but surviving bacteria in a gentamicin treatment mouse model specifically express low S10. Collectively, these data indicate that the growth arrest associated with T3SS induction can reduce antibiotic susceptibility, but cells surviving antibiotic treatment display lower levels of the exponential phase marker, S10.

Indexed as

Anti-Bacterial AgentsGentamicinsRibosomal ProteinsType III Secretion SystemsYersinia pseudotuberculosisYersinia pseudotuberculosis InfectionsAnimalsBacterial ProteinsDrug Resistance, BacterialGene Expression Regulation, BacterialMiceAnti-Bacterial AgentsBacterial ProteinsGentamicinsRibosomal ProteinsType III Secretion Systems

Identifiers

PMID40623067
PMCPMC12244630

What OpenQuestion holds

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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 OpenQuestion graph.