AraC/XylS family members, HilC and HilD, directly bind and derepress the Salmonella typhimurium hilA promoter

Roles of hilC and hilD in regulation of hilA expression in Salmonella enterica serovar Typhimurium.

Sequences between -332 and -39 upstream of the hilA promoter are required for repression of hilA. An unidentified repressor is thought to bind these upstream repressing sequences (URS) to inhibit hilA expression. Two AraC-like transcriptional regulators encoded on Salmonella pathogenicity island 1 (SPI1), HilC and HilD, bind to the URS to counteract the repression of hilA. The URS is required f...

Contribution of the RpoA C-terminal domain to stimulation of the Salmonella enterica hilA promoter by HilC and HilD.

Expression of invasion genes in Salmonella pathogenicity island 1 (SPI-1) is mainly driven by the transcriptional activator HilA. Transcription of hilA is subject to complex control and is stimulated by the SPI-1-encoded HilC and HilD proteins. The C-terminal domain of RpoA contributes to hilA activation by HilC/D under certain inducing conditions.

Serovar Typhimurium Salmonella enterica Virulence Regulatory Proteins of DNA-Binding Activities of the HilC and HilD

RtsA and RtsB coordinately regulate expression of the invasion and flagellar genes in Salmonella enterica serovar Typhimurium.

Salmonella enterica serovar Typhimurium encounters numerous host environments and defense mechanisms during the infection process. The bacterium responds by tightly regulating the expression of virulence genes. We identified two regulatory proteins, termed RtsA and RtsB, which are encoded in an operon located on an island integrated at tRNA(PheU) in S. enterica serovar Typhimurium. RtsA belongs...

HilE interacts with HilD and negatively regulates hilA transcription and expression of the Salmonella enterica serovar Typhimurium invasive phenotype.

The ability of Salmonella enterica serovar Typhimurium to traverse the intestinal mucosa of a host is an important step in its ability to initiate gastrointestinal disease. The majority of the genes required for this invasive characteristic are encoded on Salmonella pathogenicity island 1 (SPI1), and their expression is controlled by the transcriptional activator HilA, a member of the OmpR/ToxR...