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• W2125185327 startingPage "5382" @default.
• W2125185327 abstract "ABSTRACT Homeostasis of Zn 2+ and Mn 2+ is important for the physiology and virulence of the human pathogen Streptococcus pneumoniae . Here, transcriptome analysis was used to determine the response of S. pneumoniae D39 to a high concentration of Zn 2+ . Interestingly, virulence genes encoding the choline binding protein PcpA, the extracellular serine protease PrtA, and the Mn 2+ uptake system PsaBC(A) were strongly upregulated in the presence of Zn 2+ . Using random mutagenesis, a previously described Mn 2+ -responsive transcriptional repressor, PsaR, was found to mediate the observed Zn 2+ -dependent derepression. In addition, PsaR is also responsible for the Mn 2+ -dependent repression of these genes. Subsequently, we investigated how these opposite effects are mediated by the same regulator. In vitro binding of purified PsaR to the prtA , pcpA , and psaB promoters was stimulated by Mn 2+ , whereas Zn 2+ destroyed the interaction of PsaR with its target promoters. Mutational analysis of the pcpA promoter demonstrated the presence of a PsaR operator that mediates the transcriptional effects. In conclusion, PsaR is responsible for the counteracting effects of Mn 2+ and Zn 2+ on the expression of several virulence genes in S. pneumoniae , suggesting that the ratio of these metal ions exerts an important influence on pneumococcal pathogenesis." @default.
• W2125185327 created "2016-06-24" @default.
• W2125185327 creator A5001796438 @default.
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• W2125185327 creator A5054390668 @default.
• W2125185327 date "2008-08-01" @default.
• W2125185327 modified "2023-09-25" @default.
• W2125185327 title "Opposite Effects of Mn ²⁺ and Zn ²⁺ on PsaR-Mediated Expression of the Virulence Genes <i>pcpA</i> , <i>prtA</i> , and <i>psaBCA</i> of <i>Streptococcus pneumoniae</i>" @default.
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• W2125185327 doi "https://doi.org/10.1128/jb.00307-08" @default.
• W2125185327 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2493273" @default.
• W2125185327 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18515418" @default.
• W2125185327 hasPublicationYear "2008" @default.
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