ArticlePLoS pathogens2016
Fis Is Essential for Yersinia pseudotuberculosis Virulence and Protects against Reactive Oxygen Species Produced by Phagocytic Cells during Infection.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
The trial behind it
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Fis suppresses late-stage virulence gene expression in Yersinia pseudotuberculosis at environmental temperatures.PLoS pathogens · 2026Article
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- Yersinia pseudotuberculosis growth arrest during type-III secretion system expression is associated with altered ribosomal protein expression and decreased gentamicin susceptibility.PLoS pathogens · 2025Article
- Host stress drives tolerance and persistence: The bane of anti-microbial therapeutics.Cell host & microbe · 2024Review
- Article
- NO-StressedInfection and immunity · 2022Article
- Beyond dueling: roles of the type VI secretion system in microbiome modulation, pathogenesis and stress resistance.Stress biology · 2021Review
- Modifying TIMER to generate a slow-folding DsRed derivative for optimal use in quickly-dividing bacteria.PLoS pathogens · 2021Article
- Article
- Article
- Crystal structure of the nucleoid-associated protein Fis (PA4853) from Pseudomonas aeruginosa.Acta crystallographica. Section F, Structural biology communications · 2020Article
- Yersinia pseudotuberculosis YopH targets SKAP2-dependent and independent signaling pathways to block neutrophil antimicrobial mechanisms during infection.PLoS pathogens · 2020Article
- SKAP2 is required for defense againsteLife · 2020Article
- HpaR, the Repressor of Aromatic Compound Metabolism, Positively Regulates the Expression of T6SS4 to Resist Oxidative Stress inFrontiers in microbiology · 2020Article
- Amino Acid Biosynthetic Pathways Are Required forAntimicrobial agents and chemotherapy · 2019Article
- Flp, a Fis-like protein, contributes to the regulation of type III secretion and virulence processes in the phytopathogen Xanthomonas campestris pv. campestris.Molecular plant pathology · 2019Article
- Unraveling neutrophil-F1000Research · 2019Review
- CCR2Infection and immunity · 2018Article
- An Experimental Pipeline for Initial Characterization of Bacterial Type III Secretion System Inhibitor Mode of Action Using EnteropathogenicFrontiers in cellular and infection microbiology · 2018Article
- AllFrontiers in cellular and infection microbiology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
All three pathogenic Yersinia species share a conserved virulence plasmid that encodes a Type 3 Secretion System (T3SS) and its associated effector proteins. During mammalian infection, these effectors are injected into innate immune cells, where they block many bactericidal functions, including the production of reactive oxygen species (ROS). However, Y. pseudotuberculosis (Yptb) lacking the T3SS retains the ability to colonize host organs, demonstrating that chromosome-encoded factors are sufficient for growth within mammalian tissue sites. Previously we uncovered more than 30 chromosomal factors that contribute to growth of T3SS-deficient Yptb in livers. Here, a deep sequencing-based approach was used to validate and characterize the phenotype of 18 of these genes during infection by both WT and plasmid-deficient Yptb. Additionally, the fitness of these mutants was evaluated in immunocompromised mice to determine whether any genes contributed to defense against phagocytic cell restriction. Mutants containing deletions of the dusB-fis operon, which encodes the nucleoid associated protein Fis, were markedly attenuated in immunocompetent mice, but were restored for growth in mice lacking neutrophils and inflammatory monocytes, two of the major cell types responsible for restricting Yersinia infection. We determined that Fis was dispensable for secretion of T3SS effectors, but was essential for resisting ROS and regulated the transcription of several ROS-responsive genes. Strikingly, this protection was critical for virulence, as growth of ΔdusB-fis was restored in mice unable to produce ROS. These data support a model in which ROS generated by neutrophils and inflammatory monocytes that have not been translocated with T3SS effectors enter bacterial cells during infection, where their bactericidal effects are resisted in a Fis-dependent manner. This is the first report of the requirement for Fis during Yersinia infection and also highlights a novel mechanism by which Yptb defends against ROS in mammalian tissues.
Identifiers
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Registered trials
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.