FIG. 6.

Regulation of nickel transport across the H. pylori inner and outer membranes. The addition of HP1512 to the nickel regulatory network of H. pylori allows for the development of a model to explain nickel trafficking from the extracellular environment to the cytoplasm. Basal levels of nixA, HP1512, and urease expression can be adjusted to adapt to fluctuating nickel concentrations. As cytoplasmic nickel concentrations increase, nickel ions associate with cytoplasmic NikR, which confers DNA binding capabilities to NikR. Nickel-bound NikR is able to repress transcription of nixA, HP1512, and HP1400, resulting in decreased nickel uptake capacity. While the capacity to import nickel into the cytoplasm is reduced, the transcription of urease subunits is increased, resulting in the ability to utilize accumulating cytoplasmic nickel.