The PhoP/PhoQ two-component system controls the extracellular magnesium deprivation response in Salmonella enterica. In addition, several virulence-associated genes that are mainly required for intramacrophage survival during the infection process are under the control of its transcriptional regulation. Despite shared Mg 2؉ modulation of the expression of the PhoP-activated genes, no consensus sequence common to all of them could be detected in their promoter regions. We have investigated the transcriptional regulation and the interaction of the response regulator PhoP with the promoter regions of the PhoP-activated loci phoPQ, mgtA, slyB, pmrD, pcgL, phoN, pagC, and mgtCB. A direct repeat of the heptanucleotide sequence (G/T)GTTTA(A/T) was identified as the conserved motif recognized by PhoP to directly control the gene expression of the first five loci, among which the first four are ancestral to enterobacteria. On the other hand, no direct interaction of the response regulator with the promoter of phoN, pagC, or mgtCB was apparent by either in vitro or in vivo assays. These loci are Salmonella specific and were probably acquired by horizontal DNA transfer. Besides, sequence analysis of pag promoters revealed the presence of a conserved PhoP box in 6 out of the 12 genes analyzed. Our results strongly suggest that the expression of a set of Mg 2؉ -controlled genes is driven by PhoP via unknown intermediate regulatory mechanisms that could also involve ancillary factors.
The PhoP/PhoQ two-component system controls the extracellular magnesium depletion response in Salmonella enterica. Previous studies have shown that PhoP is unable to up-regulate its target genes in the absence of PhoQ function. In this work, we demonstrate that PhoP overexpression can substitute for PhoQ-and phosphorylation-dependent activation. Either a high concentration of PhoP or activation via phosphorylation stimulates PhoP self-association.
The Salmonella PmrA-PmrB system controls the expression of genes necessary for polymyxin B resistance. Four loci were previously identified as part of the regulon, and interaction of PmrA with the promoter region of three of them was observed. Here we characterized the interaction of PmrA with the promoter region of ugd, previously suggested to be regulated indirectly by PmrA. Our results indicate that PmrA controls the expression of ugd by interacting with a specific sequence in the promoter region of this gene.The two-component regulatory system PmrA-PmrB of Salmonella enterica serovar Typhimurium controls the expression of genes that mediate resistance to polymyxin B and other cationic antimicrobial polypeptides (6,8,18,22). This is accomplished by modifications of the lipopolysaccharide that result in both an increased substitution of the ester-linked phosphate at position 4Ј of the lipid A with 4-amino-4-deoxy-Larabinose (4-ARA) and also larger amounts of 2-aminoethanol esterifying the diphosphates of the core oligosaccharide (11), decreasing the binding of the antimicrobial compounds (11,19,20). Four different loci have been identified to be under control of the PmrA-PmrB system: the ugd (22) and pmrG genes (7) and the pmrCAB (22) and pmrF operons (7). ugd, also known as pmrE (7), was previously identified as pagA (17). It encodes a putative UDP-glucose dehydrogenase homologous to the products of Streptococcus pneumoniae cap3A (3) and Streptococcus pyogenes hasB (4) genes, which is responsible for the conversion of UDP-glucose into UDP-glucuronate. The pmrG gene is homologous to the ais gene of Escherichia coli (7), whose expression is aluminum induced. The pmrCAB operon encodes both the two-component system PmrA-PmrB (18) and a hydrophobic polypeptide not required for polymyxin resistance (6,21,22). The pmrF operon encodes seven polypeptides, some of which have homology to oxidoreductases, decarboxylases, and aminotransferases, that are predicted to be part of the UDP-
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