Iron-dependent transcription of the frpB gene of Helicobacter pylori is controlled by the Fur repressor protein

Abstract

We have overexpressed and purified the Helicobacter pylori Fur protein and analyzed its interaction with the intergenic regions of divergent genes involved in iron uptake (frpB and ceuE) and oxygen radical detoxification (katA and tsaA). DNase I footprint analysis showed that Fur binds specifically to a high-affinity site overlapping the P(frpB) promoter and to low-affinity sites located upstream from promoters within both the frpB-katA and ceuE-tsaA intergenic regions. Construction of an isogenic fur mutant indicated that Fur regulates transcription from the P(frpB) promoter in response to iron. In contrast, no effect by either Fur or iron was observed for the other promoters.