Affiliation:
1. Departamento de Microbiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, Mexico
Abstract
ABSTRACT
Salmonella
pathogenicity islands 1 and 2 (SPI-1 and SPI-2) have essential roles in the pathogenesis of
Salmonella enterica
. Previously, we reported transcriptional cross talk between SPI-1 and SPI-2 when the SPI-1 regulator HilD induces expression of the SsrA/B two-component system, the central positive regulator of SPI-2, during the growth of
Salmonella
to late stationary phase in LB rich medium. Here, we further define the mechanism of the HilD-mediated expression of
ssrAB
. Expression analysis of
cat
transcriptional fusions containing different regions of
ssrAB
revealed the presence of negative regulatory sequences located downstream of the
ssrAB
promoter. In the absence of these negative
cis
elements,
ssrAB
was expressed in a HilD-independent manner and was no longer repressed by the global regulator H-NS. Consistently, when the activity of H-NS was inactivated, the expression of
ssrAB
also became independent of HilD. Furthermore, electrophoretic mobility shift assays showed that both HilD and H-NS bind to the
ssrAB
region containing the repressing sequences. Moreover, HilD was able to displace H-NS bound to this region, whereas H-NS did not displace HilD. Our results support a model indicating that HilD displaces H-NS from a region downstream of the promoter of
ssrAB
by binding to sites overlapping or close to those sites bound by H-NS, which leads to the expression of
ssrAB
. Although the role of HilD as an antagonist of H-NS has been reported before for other genes, this is the first study showing that HilD is able to effectively displace H-NS from the promoter of one of its target genes.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology