Member of the two-component regulatory system PhoP/PhoQ involved in adaptation to low Mg(2+) environments and the control of acid resistance genes. In low periplasmic Mg(2+), PhoQ phosphorylates PhoP, resulting in the expression of PhoP-activated genes (PAG) and repression of PhoP-repressed genes (PRG). In high periplasmic Mg(2+), PhoQ dephosphorylates phospho-PhoP, resulting in the repression of PAG and may lead to expression of some PRG (By similarity). Mediates magnesium influx to the cytosol by activation of MgtA. Promotes expression of the two-component regulatory system rstA/rstB and transcription of the hemL, mgrB, nagA, slyB, vboR and yrbL genes. Feedback inhibited by MgrB, which seems to bind PhoQ, altering its activity and that of downstream effector PhoP. PhoP-regulated transcription is redox-sensitive, being activated when the periplasm becomes more reducing (deletion of dsbA/dsbB, or treatment with dithiothreitol). MgrB acts between DsbA/DsbB and PhoP/PhoQ in this pathway. Monomer in the inactive, unphosphorylated state and dimer in the active, phosphorylated state. The phoP/phoQ operon is positively autoregulated by both PhoP and PhoQ in a Mg(2+)-dependent manner, inhibited at high Mg(2+) concentrations (PubMed:10464230). Induced by dsbA disruption and dithiothreitol (PubMed:22267510). Phosphorylated by PhoQ. Altered expression of 33 genes; 9 are down-regulated, the rest up-regulated. There is a close linkage between the Rcs and PhoQ/P signaling systems, and both signaling systems respond to certain external divalent cations (zinc and magnesium). Two-component regulatory system EvgA/EvgS interacts with PhoP/PhoQ via signal transduction mediated by phospho-EvgA.