The role and regulation of the phosphohistidine phosphatase sixA in the starvation-stress response of Salmonella enterica serovar typhimurium.

摘要

The metabolic changes that Salmonella undergoes during carbon-energy starvation are known as the starvation-stress response (SSR). We hypothesized that the sixA gene product regulates the phosphorylation status of one or more response regulators during the SSR and is regulated by the sigma factor sigmaE. Wild type and sixA null mutant strains were compared for their abilities to: survive long-term C-starvation and develop C-starvation-induced cross-resistance to environmental stresses. Also, sixA gene expression was measured in wild type, rpoE, rpoS, and rpoE rpoS backgrounds. Our results showed that a sixA null mutation increases CSI cross-resistance to polymyxin-B and reduces CSI cross-resistance to H2O2 and possibly pH 3.3 in 5-h C-starved cells and reduces C-starvation-survival. In contrast, sixA did not have a significant effect on CSI cross-resistances in 24-h C-starved cells. Furthermore, sixA is induced in a sigma E-dependent manner in 5-h C-starved cells and (indirectly) repressed in a sigmaS-dependent manner in 24-h C-starved cells.