ArticlePloS one2014
Role of pathogenicity determinant protein C (PdpC) in determining the virulence of the Francisella tularensis subspecies tularensis SCHU.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- 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
- Atomic Structure and Phospholipid Binding Properties of thebioRxiv : the preprint server for biology · 2025Article
- Phenotypic and transcriptional characterization ofFrontiers in microbiology · 2024Article
- The intracellular pathogenLife science alliance · 2022Article
- Type VI Secretion System and Its Effectors PdpC, PdpD, and OpiA Contribute toInfection and immunity · 2021Article
- Identification of an Attenuated Substrain ofPathogens (Basel, Switzerland) · 2021Article
- 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
- Protective effects of the Francisella tularensis ΔpdpC mutant against its virulent parental strain SCHU P9 in Cynomolgus macaques.Scientific reports · 2019Article
- Expression of Francisella pathogenicity island protein intracellular growth locus E (IglE) in mammalian cells is involved in intracellular trafficking, possibly through microtubule organizing center.MicrobiologyOpen · 2019Article
- Article
- TheFrontiers in cellular and infection microbiology · 2018Review
- Francisella requires dynamic type VI secretion system and ClpB to deliver effectors for phagosomal escape.Nature communications · 2017Article
- Symbiosis with Francisella tularensis provides resistance to pathogens in the silkworm.Scientific reports · 2016Article
- Pullulanase Is Necessary for the Efficient Intracellular Growth of Francisella tularensis.PloS one · 2016Article
- Use of aminoglycoside 3' adenyltransferase as a selection marker for Chlamydia trachomatis intron-mutagenesis and in vivo intron stability.BMC research notes · 2015Article
- Identification of mechanisms for attenuation of the FSC043 mutant of Francisella tularensis SCHU S4.Infection and immunity · 2014Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Francisella tularensis subspecies tularensis, the etiological agent of tularemia, is highly pathogenic to humans and animals. However, the SCHU strain of F. tularensis SCHU P0 maintained by passaging in artificial media has been found to be attenuated. To better understand the molecular mechanisms behind the pathogenicity of F. tularensis SCHU, we attempted to isolate virulent bacteria by serial passages in mice. SCHU P5 obtained after 5th passages in mice remained avirulent, while SCHU P9 obtained after 9th passages was completely virulent in mice. Moreover, SCHU P9 grew more efficiently in J774.1 murine macrophages compared with that in the less pathogenic SCHU P0 and P5. Comparison of the nucleotide sequences of the whole genomes of SCHU P0, P5, and P9 revealed only 1 nucleotide difference among P0, P5 and P9 in 1 of the 2 copies of pathogenicity determinant protein C (pdpC) gene. An adenine residue deletion was observed in the pdpC1 gene of SCHU P0, P5, and P9 and in the pdpC2 gene of SCHU P0, and P5, while P9 was characterized by the wild type pdpC2 gene. Thus, SCHU P0 and P5 expressed only truncated forms of PdpC protein, while SCHU P9 expressed both wild type and truncated versions. To validate the pathogenicity of PdpC, both copies of the pdpC gene in SCHU P9 have been inactivated by Targetron mutagenesis. SCHU P9 mutants with inactivated pdpC gene showed low intracellular growth in J774.1 cells and did not induce severe disease in experimentally infected mice, while virulence of the mutants was restored by complementation with expression of the intact PdpC. These results demonstrate that PdpC is crucial in determining the virulence of F. tularensis SCHU.
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