Regulation of Salmonella enterica pathogenicity island 1 (SPI‐1) by the LysR‐type regulator LeuO. Issue 6 (13th January 2014)

• Record Type: Journal Article
• Authors: Espinosa, Elena; Casadesús, Josep
• Is Part Of: Molecular microbiology. Volume 91:Issue 6(2014)
• Page Start: 1057
• Page End: 1069
• Publication Date: 2014-01-13
• Subjects: Molecular microbiology -- Periodicals; 572.829
• DOI: 10.1111/mmi.12500
• Languages: English
• ISSNs: 0950-382X

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>LeuO is a quiescent LysR‐type regulator belonging to the H‐NS regulon. Activation of <italic>leuO</italic> transcription represses expression of pathogenicity island 1 (SPI‐1) in <italic>S</italic><italic>almonella enterica</italic> serovar Typhimurium and inhibits invasion of epithelial cells. Loss of HilE suppresses LeuO‐mediated downregulation of SPI‐1. Activation of <italic>leuO</italic> transcription reduces the level of HilD protein, and loss of HilE restores the wild type HilD level. Hence, LeuO‐mediated downregulation of SPI‐1 may involve inhibition of HilD activity by HilE, a view consistent with the fact that HilE is a HilD inhibitor. <italic>In vivo</italic> analyses using β‐galactosidase fusions indicate that LeuO activates <italic>hilE</italic> transcription. <italic>In vitro</italic> analyses by slot blotting, electrophoretic mobility shift analysis and DNase I footprinting show that LeuO binds the <italic>hilE</italic> promoter region. Although residual SPI‐1 repression by LeuO is observed in the absence of HilE, the LeuO‐HilE‐HilD 'pathway' appears to be the major mechanism. Because both <italic>leuO</italic> and SPI‐1 are repressed by H‐NS, activation of <italic>leuO</italic> transcription may provide a backup mechanism for SPI‐1 repression under conditions that impair H‐NS‐mediated silencing.</p> </abstract>