ArticleFrontiers in microbiology2015
Host cell type-dependent translocation and PhoP-mediated positive regulation of the effector SseK1 of Salmonella enterica.
Article in Frontiers in microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Similar Virulence Gene Repertoires but Distinct Stress Tolerance and Pathogenicity-Associated Phenotypes in RepresentativeMicroorganisms · 2026Article
- Salmonella T3SS effector SseK1 arginine-glycosylates the two-component response regulator OmpR to alter bile salt resistance.Scientific reports · 2023Article
- Speaking the host language: howMicrobiology (Reading, England) · 2023Review
- Novel Template Plasmids pCyaA'-Kan and pCyaA'-Cam for Generation of Unmarked ChromosomalMicroorganisms · 2021Article
- Arginine glycosylation enhances methylglyoxal detoxification.Scientific reports · 2021Article
- Tubulin Folding Cofactor TBCB is a Target of theInternational journal of molecular sciences · 2020Article
- Type III Secretion Effectors with Arginine N-Glycosyltransferase Activity.Microorganisms · 2020Review
- Arg-GlcNAcylation on TRADD by NleB and SseK1 Is Crucial for Bacterial Pathogenesis.Frontiers in cell and developmental biology · 2020Article
- A LivemSphere · 2019Article
- A Novel PhoP/PhoQ Regulation Pathway Modulates the Survival of Extraintestinal PathogenicFrontiers in immunology · 2018Article
- Dual Expression of theFrontiers in microbiology · 2017Article
Corrections and comments
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Authors and funding
3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Salmonella enterica expresses two virulence-related type III secretion systems (T3SSs) encoded in Salmonella pathogenicity island 1 (SPI1) and SPI2, respectively. SseK1 is a poorly characterized substrate of the SPI2-encoded T3SS. Here, we show that this effector is essential to get full virulence both in oral and intraperitoneal mice infections, in spite of not having a role in invasion or intracellular proliferation in cultured mammalian cells. In vitro, expression of sseK1 was higher in media mimicking intracellular conditions, when SPI2 was induced, but it was also significant under SPI1 inducing conditions. A detailed analysis of translocation of SseK1 into host cells unveiled that it was a substrate of both, T3SS1 and T3SS2, although with different patterns and kinetics depending on the specific host cell type (epithelial, macrophages, or fibroblasts). The regulation of the expression of sseK1 was examined using lacZ and bioluminescent lux fusions. The two-component system PhoQ/PhoP is a positive regulator of this gene. A combination of sequence analysis, directed mutagenesis and electrophoretic mobility shift assays showed that phosphorylated PhoP binds directly to the promoter region of sseK1 and revealed a PhoP binding site located upstream of the predicted -35 hexamer of this promoter.
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