Acetylation of Lysine 201 Inhibits the DNA-Binding Ability of PhoP to Regulate Salmonella Virulence

摘要: The two-component system PhoP-PhoQ is highly conserved in bacteria and regulates virulence response to various signals for within the mammalian host. Here, we demonstrate that PhoP could be acetylated by Pat deacetylated deacetylase CobB enzymatically vitro vivo Salmonella Typhimurium. Specifically, lysine residue 201(K201) winged helix-turn-helix motif at C-terminal DNA-binding domain of acetylated, its acetylation level decreases dramatically when encounter low magnesium, acid stress or phagocytosis macrophages. has a decreased increased ability deletion mutant pat. However, K201 does not counteract phosphorylation, which essential activity. In addition, (mimicked glutamine substitute) S. Typhimurium causes significantly attenuated intestinal inflammation as well systemic infection mouse model, suggesting deacetylation pathogenesis. Therefore, propose reversible may ensure promptly respond different stresses host cells. These findings suggest domain, novel regulatory mechanism gene expression, involved bacterial across microorganisms.