Nickel is an essential transition metal for the virulence and survival of Helicobacter pylori in the acidic human stomach. The nickel– and proton– dependent transcriptional regulator HpNikR is important for maintaining nickel homeostasis inside the cytosol by regulating multiple H. pylori genes. A previous ChIP-sequencing experiment with H. pylori G27 and HpNikR identified two novel genes currently annotated as putative iron-transporters, HpG27_866 and HpG27_1499. In vitro DNA-binding assays with the promoter sequences of the two genes revealed nickel-dependent HpNikR binding with an affinity of ~10-7 M. The recognition site of HpNikR was identified on HpG27_1499 by footprinting assays, which loosely correlates with the HpNikR pseudo-consensus sequence. Furthermore, HpG27_1499 transcription showed nickel-dependent repression in WT H. pylori, and no changes in an isogenic ΔnikR strain. These data suggest that HpG27_1499 could be a nickel importer that is regulated by HpNikR in a nickel-responsive manner.

Nickel is an essential transition metal for the virulence and survival of Helicobacter pylori in the acidic human stomach. The nickel– and proton– dependent transcriptional regulator HpNikR is important for maintaining nickel homeostasis inside the cytosol by regulating multiple H. pylori genes. A previous ChIP-sequencing experiment with H. pylori G27 and HpNikR identified two novel genes currently annotated as putative iron-transporters, HpG27_866 and HpG27_1499. In vitro DNA-binding assays with the promoter sequences of the two genes revealed nickel-dependent HpNikR binding with an affinity of ~10-7 M. The recognition site of HpNikR was identified on HpG27_1499 by footprinting assays, which loosely correlates with the HpNikR pseudo-consensus sequence. Furthermore, HpG27_1499 transcription showed nickel-dependent repression in WT H. pylori, and no changes in an isogenic ΔnikR strain. These data suggest that HpG27_1499 could be a nickel importer that is regulated by HpNikR in a nickel-responsive manner.