The response regulator SsrB activates transcription and binds to a region overlapping OmpR binding sites atSalmonellapathogenicity island 2.

OmpR activates expression of the two-component regulatory system located onSalmonellapathogenicity island 2 (SPI-2) that controls the expression of a type III secretion system, as well as many other genes required for systemic infection in mice. Measurements of SsrA and SsrB protein levels under different growth conditions indicate that expression of these two components is uncoupled, i.e. SsrB is produced in the absence ofssrAand vice versa. This result was suggested from our previous studies, in which two promoters atssrA/Bwere identified. The isolated C-terminus of SsrB binds to DNA and protects regions upstream ofssrA,ssrBandsrfHfrom DNase I digestion. Furthermore, the C-terminus of SsrB alone is capable of activating transcription in the absence of the N-terminus. Results fromβ-galactosidase assays indicate that the N-terminal phosphorylation domain inhibits the C-terminal effector domain. A previous study from our laboratory reported thatssrA–lacZandssrB–lacZtranscriptional fusions were substantially reduced in anssrBnull strain. Results from DNase I protection assays provide direct evidence that SsrB binds atssrAandssrB, although the binding sites lie within the transcribed regions. Additional regulators clearly affect gene expression at this important locus, and here we provide evidence that SlyA, a transcription factor that contributes toSalmonellavirulence, also affectsssrA/Bgene expression. [ABSTRACT FROM AUTHOR]