PhoP Induced Genes within Salmonella Pathogenicity Island 1

AGUIRRE, A.; CABEZA, M. L.; SPINELLI, S. V.; MCCLELLAND, M.; GARCÍA VÉSCOVI, E.; SONCINI, F.

Orlando, USA

Congreso; 106th General Meeting of the American Society for Microbiology; 2006

American Society for Microbiology

The invasive pathogen Salmonella enterica has evolved a sophisticated device that allows it to enter non-phagocytic host cells. This process requires the expression of the Salmonella pathogenicity island 1 (SPI-1), that encodes a specialized type III protein secretion system (TTSS). This TTSS delivers a set of effectors that produce a marked rearrangement of the host-cell cytoskeleton, generating a profuse membrane ruffling at the site of interaction, driving bacterial entry. It has been shown that the PhoP/PhoQ two-component system represses the expression of the SPI-1 machinery, by affecting the transcription of its master regulator HilA. We describe here a PhoP-activated transcriptional unit within SPI-1. This transcriptional unit is composed by the orgB and orgC genes, which encode a protein that interacts with the InvC ATPase, and a putative effector protein of this TTSS, respectively. Expression of these two genes is directly controlled by the phosphorylated form of PhoP, which recognizes a PhoP-box located at the -35 region relative to a new discovered transcription start site within the 3’ coding region of the upstream gene orgA. Furthermore, expression of this locus is only slightly affected by the disruption of the SPI-1 master regulator coding gene, hilA, or by polar insertions located at prgH or at the 5’ region of orgA, upstream the orgBC transcription start site and the PhoP-recognition sequence. Because HilA promotes the expression of its target genes in invasion-inducing conditions and PhoP/PhoQ activates its regulon upon Salmonella entry into the host cells, these results indicate that orgB and orgC are both expressed during the host cell invasion, by the HilA-controlled promoter located upstream prgH, and after the internalization, by the PhoP/PhoQ-controlled promoter. Altogether these observations suggest a role of OrgB and OrgC after the host-cell entry.