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The TviA auxiliary protein renders the Salmonella enterica serotype Typhi RcsB regulon responsive to changes in osmolarity
Author(s) -
Winter Sebastian E.,
Winter Maria G.,
Thiennimitr Parameth,
Gerriets Valerie A.,
Nuccio SeanPaul,
Rüssmann Holger,
Bäumler Andreas J.
Publication year - 2009
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.1365-2958.2009.06859.x
Subject(s) - biology , regulon , salmonella enterica , microbiology and biotechnology , protein data bank (rcsb pdb) , flagellum , regulation of gene expression , gene , genetics , escherichia coli , biochemistry
Summary In response to osmolarity, Salmonella enterica serotype Typhi ( S. Typhi) regulates genes required for Vi capsular antigen expression oppositely to those required for motility and invasion. Previous studies suggest that osmoregulation of motility, invasion and capsule expression is mediated through the RcsC/RcsD/RcsB phosphorelay system. Here we performed gene expression profiling and functional studies to determine the role of TviA, an auxiliary protein of the RcsB response regulator, in controlling virulence gene expression in S. Typhi. TviA repressed expression of genes encoding flagella and the invasion‐associated type III secretion system (T3SS‐1) through repression of the flagellar regulators flhDC and fliZ , resulting in reduced invasion, reduced motility and reduced expression of FliC. Both RcsB and TviA repressed expression of flhDC , but only TviA altered flhDC expression in response to osmolarity. Introduction of tviA into S. enterica serotype Typhimurium rendered flhDC transcription sensitive to changes in osmolarity. These data suggest that the auxiliary TviA protein integrates a new regulatory input into the RcsB regulon of S. Typhi, thereby altering expression of genes encoding flagella, the Vi antigen and T3SS‐1 in response to osmolarity.