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• W2026248970 endingPage "1509" @default.
• W2026248970 startingPage "1497" @default.
• W2026248970 abstract "Salmonella enterica serovar Typhimurium requires the type III secretion system encoded by Salmonella pathogenicity island 1 (SPI1) and controlled by the master regulator, HilA, to penetrate the intestinal epithelium. Numerous regulators affect virulence through influence on this system, including the proteolytic component ClpP, the stationary phase regulator RpoS and the carbon-storage regulator CsrA. However, the mechanism behind the ClpP regulation is not fully understood. To elucidate this we examined differentially expressed genes in a ΔclpP mutant compared with WT using global transcriptomic analysis. SPI1 and SPI4 virulence genes were significantly downregulated in the ΔclpP mutant, whereas several RpoS-dependent genes and the fliC gene encoding flagellin were upregulated. While the ΔclpP mutant was attenuated in cell invasion, this attenuation was not present in a ΔclpP/rpoS : : amp double mutant, suggesting the repression of invasion was directed through RpoS. The expression of the csrA virulence regulator was increased in the ΔclpP mutant and decreased in the rpoS : : amp and ΔclpP/rpoS : : amp mutants, indicating that ClpP affects the csrA expression level as well. Thus, this study suggests that ClpP affects SPI1 expression and thereby virulence indirectly through its regulation of both RpoS and CsrA." @default.
• W2026248970 created "2016-06-24" @default.
• W2026248970 creator A5012915369 @default.
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• W2026248970 creator A5030061489 @default.
• W2026248970 creator A5068369120 @default.
• W2026248970 creator A5073008185 @default.
• W2026248970 date "2013-07-01" @default.
• W2026248970 modified "2023-10-14" @default.
• W2026248970 title "ClpP deletion causes attenuation of Salmonella Typhimurium virulence through mis-regulation of RpoS and indirect control of CsrA and the SPI genes" @default.
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• W2026248970 doi "https://doi.org/10.1099/mic.0.065797-0" @default.
• W2026248970 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23676436" @default.
• W2026248970 hasPublicationYear "2013" @default.
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