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AraC/XylS family members, HilD and HilC, directly activate virulence gene expression independently of HilA in Salmonella typhimurium
Author(s) -
Akbar Samina,
Schechter Lisa M.,
Lostroh C. Phoebe,
Lee Catherine A.
Publication year - 2003
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.1365-2958.2003.03322.x
Subject(s) - pathogenicity island , biology , gene , transcription factor , secretion , microbiology and biotechnology , virulence , transcription (linguistics) , type three secretion system , genetics , regulation of gene expression , biochemistry , linguistics , philosophy
Summary Salmonella typhimuriumis a Gram‐negative enteric pathogen that can infect intestinal epithelial cells and induce inflammation of the intestinal mucosa. These processes are mediated by a type III secretion system (TTSS), which is encoded onSalmonellapathogenicity island 1 (SPI1). Previous studies showed that four SPI1‐encoded transcriptional regulators, HilD, HilC, HilA and InvF, act in an ordered fashion to co‐ordinately activate expression of the SPI1 TTSS. HilD and HilC derepresshilAtranscription. HilA activatesinvFas well as SPI1 genes that encode components of the TTS apparatus. InvF then activates genes that encode proteins secreted by the SPI1 TTS apparatus. In this scheme, HilD and HilC indirectly activate expression of the SPI1 TTS apparatus and its secreted substrates by affectinghilAexpression. Here, we report that HilD and HilC can also activate expression of a subset of SPI1 genes independently of HilA. Our studies show that HilD and HilC activate transcription ofinvFfrom a promoter that is far upstream of its HilA‐dependent promoter. This activation is most probably through direct binding of HilD and HilC to sequences upstream and downstream of this alternative HilA‐independent promoter. We conclude that HilD and HilC have a second role in SPI1 gene regulation that is separate from their role in co‐ordinating expression of the SPI1 TTSS throughhilA .