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RcsB‐BglJ activates the Escherichia coli leuO gene, encoding an H‐NS antagonist and pleiotropic regulator of virulence determinants
Author(s) -
Stratmann Thomas,
Pul Ümit,
Wurm Reinhild,
Wagner Rolf,
Schnetz Karin
Publication year - 2012
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2012.07993.x
Subject(s) - protein data bank (rcsb pdb) , repressor , biology , psychological repression , gene , transcription factor , genetics , transcription (linguistics) , pathogenicity island , promoter , regulator , transcriptional regulation , regulation of gene expression , escherichia coli , virulence , gene expression , biochemistry , linguistics , philosophy
Summary The LysR‐type transcription factor LeuO is involved in regulation of pathogenicity determinants and stress responses in Enterobacteriaceae, and acts as antagonist of the global repressor H‐NS. Expression of the leuO gene is repressed by H‐NS, and it is upregulated in stationary phase and under amino acid starvation conditions. Here, we show that the heterodimer of the FixJ/NarL‐type transcription regulators RcsB and BglJ strongly activates expression of leuO and that RcsB‐BglJ regulates additional loci. Activation of leuO by RcsB‐BglJ is independent of the Rcs phosphorelay system. RcsB‐BglJ binds to the leuO promoter region and activates one of two leuO promoters mapped in vivo . Moreover, LeuO antagonizes activation of leuO by RcsB‐BglJ and acts as negative autoregulator in vivo and in vitro . Further, the H‐NS paralogue StpA causes repression of leuO in addition to H‐NS. Together, our data suggest a complex arrangement of regulatory elements and they indicate a feedback control mechanism of leuO expression.

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