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- W1703062912 abstract "Salmonella enterica can cause intestinal or systemic infections in humans and animals mainly by the presence of pathogenicity islands SPI-1 and SPI-2, containing 39 and 44 genes, respectively. The AraC-like regulator HilD positively controls the expression of the SPI-1 genes, as well as many other Salmonella virulence genes including those located in SPI-2. A previous report indicates that the two-component system CpxR/A regulates the SPI-1 genes: the absence of the sensor kinase CpxA, but not the absence of its cognate response regulator CpxR, reduces their expression. The presence and absence of cell envelope stress activates kinase and phosphatase activities of CpxA, respectively, which in turn controls the level of phosphorylated CpxR (CpxR-P). In this work, we further define the mechanism for the CpxR/A-mediated regulation of SPI-1 genes. The negative effect exerted by the absence of CpxA on the expression of SPI-1 genes was counteracted by the absence of CpxR or by the absence of the two enzymes, AckA and Pta, which render acetyl-phosphate that phosphorylates CpxR. Furthermore, overexpression of the lipoprotein NlpE, which activates CpxA kinase activity on CpxR, or overexpression of CpxR, repressed the expression of SPI-1 genes. Thus, our results provide several lines of evidence strongly supporting that the absence of CpxA leads to the phosphorylation of CpxR via the AckA/Pta enzymes, which represses both the SPI-1 and SPI-2 genes. Additionally, we show that in the absence of the Lon protease, which degrades HilD, the CpxR-P-mediated repression of the SPI-1 genes is mostly lost; moreover, we demonstrate that CpxR-P negatively affects the stability of HilD and thus decreases the expression of HilD-target genes, such as hilD itself and hilA, located in SPI-1. Our data further expand the insight on the different regulatory pathways for gene expression involving CpxR/A and on the complex regulatory network governing virulence in Salmonella." @default.
- W1703062912 created "2016-06-24" @default.
- W1703062912 creator A5001419706 @default.
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- W1703062912 creator A5040809790 @default.
- W1703062912 creator A5044816776 @default.
- W1703062912 creator A5078854040 @default.
- W1703062912 date "2015-08-06" @default.
- W1703062912 modified "2023-10-11" @default.
- W1703062912 title "The two-component system CpxR/A represses the expression of Salmonella virulence genes by affecting the stability of the transcriptional regulator HilD" @default.
- W1703062912 cites W1638049493 @default.
- W1703062912 cites W1724694855 @default.
- W1703062912 cites W1757579909 @default.
- W1703062912 cites W1817288881 @default.
- W1703062912 cites W1849830312 @default.
- W1703062912 cites W1938034723 @default.
- W1703062912 cites W1968846062 @default.
- W1703062912 cites W1970934009 @default.
- W1703062912 cites W1973552999 @default.
- W1703062912 cites W1973974403 @default.
- W1703062912 cites W1975809728 @default.
- W1703062912 cites W1977836482 @default.
- W1703062912 cites W1979740345 @default.
- W1703062912 cites W1985963323 @default.
- W1703062912 cites W1988717370 @default.
- W1703062912 cites W1993995188 @default.
- W1703062912 cites W1995887685 @default.
- W1703062912 cites W2001740561 @default.
- W1703062912 cites W2003729219 @default.
- W1703062912 cites W2004476295 @default.
- W1703062912 cites W2005008281 @default.
- W1703062912 cites W2006252065 @default.
- W1703062912 cites W2007114933 @default.
- W1703062912 cites W2029348973 @default.
- W1703062912 cites W2031678726 @default.
- W1703062912 cites W2033792964 @default.
- W1703062912 cites W2046193812 @default.
- W1703062912 cites W2051048419 @default.
- W1703062912 cites W2061997872 @default.
- W1703062912 cites W2071999738 @default.
- W1703062912 cites W2079025858 @default.
- W1703062912 cites W2079748997 @default.
- W1703062912 cites W2090097918 @default.
- W1703062912 cites W2092314606 @default.
- W1703062912 cites W2094005790 @default.
- W1703062912 cites W2094411666 @default.
- W1703062912 cites W2095836360 @default.
- W1703062912 cites W2096053073 @default.
- W1703062912 cites W2097888283 @default.
- W1703062912 cites W2101279843 @default.
- W1703062912 cites W2101292502 @default.
- W1703062912 cites W2105208278 @default.
- W1703062912 cites W2106171353 @default.
- W1703062912 cites W2108145381 @default.
- W1703062912 cites W2109355889 @default.
- W1703062912 cites W2110412791 @default.
- W1703062912 cites W2111879055 @default.
- W1703062912 cites W2114302840 @default.
- W1703062912 cites W2114719101 @default.
- W1703062912 cites W2115490768 @default.
- W1703062912 cites W2115493975 @default.
- W1703062912 cites W2115775744 @default.
- W1703062912 cites W2116137883 @default.
- W1703062912 cites W2116226435 @default.
- W1703062912 cites W2117805957 @default.
- W1703062912 cites W2120926466 @default.
- W1703062912 cites W2121396317 @default.
- W1703062912 cites W2122343132 @default.
- W1703062912 cites W2123456207 @default.
- W1703062912 cites W2123484637 @default.
- W1703062912 cites W2123724054 @default.
- W1703062912 cites W2125172023 @default.
- W1703062912 cites W2127041383 @default.
- W1703062912 cites W2127697422 @default.
- W1703062912 cites W2128896236 @default.
- W1703062912 cites W2129099337 @default.
- W1703062912 cites W2130036880 @default.
- W1703062912 cites W2133342418 @default.
- W1703062912 cites W2134486319 @default.
- W1703062912 cites W2135182617 @default.
- W1703062912 cites W2137678717 @default.
- W1703062912 cites W2140162925 @default.
- W1703062912 cites W2142424488 @default.
- W1703062912 cites W2142863488 @default.
- W1703062912 cites W2147189708 @default.
- W1703062912 cites W2148749184 @default.
- W1703062912 cites W2151026417 @default.
- W1703062912 cites W2151405008 @default.
- W1703062912 cites W2159612861 @default.
- W1703062912 cites W2159671439 @default.
- W1703062912 cites W2160174395 @default.
- W1703062912 cites W2161973127 @default.
- W1703062912 cites W2163258677 @default.
- W1703062912 cites W2168365932 @default.
- W1703062912 cites W2172112954 @default.
- W1703062912 doi "https://doi.org/10.3389/fmicb.2015.00807" @default.
- W1703062912 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4526804" @default.
- W1703062912 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26300871" @default.
- W1703062912 hasPublicationYear "2015" @default.
- W1703062912 type Work @default.