ArticleInfection and immunity2013
Disruption of Francisella tularensis Schu S4 iglI, iglJ, and pdpC genes results in attenuation for growth in human macrophages and in vivo virulence in mice and reveals a unique phenotype for pdpC.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
- Dual host and pathogen targeting by MEK1/2 inhibitors.Infection and immunity · 2026Review
- Structure and potential role of T6SS effector PdpC in Francisella tularensis intracellular lifestyle.Communications biology · 2026Article
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- Type VI secretion systems at the interface between bacteria and eukaryotic cells.Genetics and molecular biology · 2026Article
- Targeting the MEK1/2 pathway to combatmBio · 2025Article
- Atomic Structure and Phospholipid Binding Properties of thebioRxiv : the preprint server for biology · 2025Article
- Identification of the Francisella novicida FTN_0096 as a factor involved in intracellular replication and host response.PloS one · 2025Article
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- SPA Promotes Atherosclerosis Through Mediating Macrophage Foam Cell Formation-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- A novel method of Francisella infection of epithelial cells using HeLa cells expressing fc gamma receptor.BMC infectious diseases · 2024Article
- Killing in the name of: T6SS structure and effector diversity.Microbiology (Reading, England) · 2023Review
- PdpC, a secreted effector protein of the type six secretion system, is required for erythrocyte invasion byFrontiers in cellular and infection microbiology · 2022Article
- Type VI Secretion System and Its Effectors PdpC, PdpD, and OpiA Contribute toInfection and immunity · 2021Article
- Using proteomics to identify host cell interaction partners for VgrG and IglJ.Scientific reports · 2020Article
- OpiA, a Type Six Secretion System Substrate, Localizes to the Cell Pole and Plays a Role in Bacterial Growth and Viability inJournal of bacteriology · 2020Article
- An Overview of Anti-Eukaryotic T6SS Effectors.Frontiers in cellular and infection microbiology · 2020Review
- Article
- Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019Review
- TheFrontiers in cellular and infection microbiology · 2018Review
- Complement C3 as a Prompt for Human Macrophage Death during Infection with Francisella tularensis Strain SCHU S4.Infection and immunity · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Francisella tularensis is a facultative intracellular bacterial pathogen and the causative agent of tularemia. After infection of macrophages, the organism escapes from its phagosome and replicates to high density in the cytosol, but the bacterial factors required for these aspects of virulence are incompletely defined. Here, we describe the isolation and characterization of Francisella tularensis subsp. tularensis strain Schu S4 mutants that lack functional iglI, iglJ, or pdpC, three genes of the Francisella pathogenicity island. Our data demonstrate that these mutants were defective for replication in primary human monocyte-derived macrophages and murine J774 cells yet exhibited two distinct phenotypes. The iglI and iglJ mutants were similar to one another, exhibited profound defects in phagosome escape and intracellular growth, and appeared to be trapped in cathepsin D-positive phagolysosomes. Conversely, the pdpC mutant avoided trafficking to lysosomes, phagosome escape was diminished but not ablated, and these organisms replicated in a small subset of infected macrophages. The phenotype of each mutant strain was reversed by trans complementation. In vivo virulence was assessed by intranasal infection of BALB/c mice. The mutants appeared avirulent, as all mice survived infection with 10(8) CFU iglJ- or pdpC-deficient bacteria. Nevertheless, the pdpC mutant disseminated to the liver and spleen before being eliminated, whereas the iglJ mutant did not. Taken together, our data demonstrate that the pathogenicity island genes tested are essential for F. tularensis Schu S4 virulence and further suggest that pdpC may play a unique role in this process, as indicated by its distinct intermediate phenotype.
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