Premium
Transcriptional activation of Salmonella typhimurium invasion genes by a member of the phosphorylated response‐regulator superfamily
Author(s) -
Johnston Christine,
Pegues David A.,
Hueck Christoph J.,
Lee Catherine A.,
Miller Samuel I.
Publication year - 1996
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 - 10.1046/j.1365-2958.1996.d01-1719.x
Subject(s) - biology , pathogenicity island , response regulator , gene , secretion , transcription (linguistics) , transcription factor , type three secretion system , mutant , locus (genetics) , genetics , microbiology and biotechnology , escherichia coli , biochemistry , linguistics , philosophy
The Salmonella typhimurium PhoP‐repressed locus prgHIJK encodes components of a sec‐ independent type III secretion apparatus. This apparatus is composed of at least 17 proteins encoded on a 40kb pathogenicity island located at centisome 63 on the S. typhimurium chromosome. The secretion apparatus and some of its targets, SspB, SspC and SspD, are necessary for epithelial cell invasion. The transcription of many invasion genes, including prgHIJK , is co‐ordinately activated by HilA, a transcription factor encoded within the pathogenicity island. In this report we identify sirA , a gene located outside the pathogenicity island that is essential for induction of prgHIJK and hilA transcription. sirA encodes a 234‐amino‐acid protein that is essential for S. typhimurium Ssp ( Salmonella secreted protein) secretion and invasion and is similar to response regulators of two‐component regulatory systems. sirA ‐mutant phenotypes could be suppressed by two DNA clones from unlinked loci, designated sirB and sirC . These data suggest that SirA may be phosphorylated in response to S. typhimurium sensing a mammalian microenvironment. Furthermore, SirA phosphorylation is predicted to initiate a cascade of transcription‐factor synthesis which results in invasion‐gene transcription, Ssp secretion, and bacterial invasion of epithelia.