| Summary: | <p>Abstract</p> <p>Background</p> <p>The survival of <it>Salmonella enterica </it>within the intracellular host niche requires highly co-ordinated expression of virulence effectors predominantly regulated by the SsrAB two-component regulatory system. <it>S. enterica </it>serovar Typhimurium mutants lacking the <it>ssrAB </it>genes are avirulent in mice, highlighting the importance of this regulatory system <it>in vivo</it>. Mutants lacking the gene encoding the alternative sigma factor σ<sup>E </sup>(<it>rpoE</it>) are also highly attenuated for intracellular survival, pointing to a potential connection with the SsrAB regulatory system.</p> <p>Results</p> <p>In this study we demonstrate that RpoE is involved in fine-tuning the expression of a subset of SsrB-regulated genes found in the <it>Salmonella </it>pathogenicity island-2 (SPI-2) genetic locus that encodes a horizontally acquired type III secretion system, and unlinked genes integrated into this regulon that are required for virulence in host animals.</p> <p>Conclusion</p> <p>These data point to a potential connection between the virulence phenotype of strains lacking <it>ssrB </it>and <it>rpoE</it>, and highlight new transcriptional regulation that might be essential for appropriate temporal and spatial control of the virulence-associated type III secretion system during host infection.</p>
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