Abstract
Transcription of both chromosomal and extrachromosomally introduced nifS was regulated (up-expressed) by oxygen or by supplemental iron conditions. This up-expression was not observed in a fur mutant strain background or when an iron chelator was added. Iron-bound Fur (but not apo-Fur) recognized the nifS promoter, and Fur bound significantly farther upstream (-155 bp to -190 bp and -210 to -240 bp) in the promoter than documented Helicobacter pylori Fur binding regions. This binding was stronger than Fur recognition of the flgE or napA promoter and includes a Fur recognition sequence common to the H. pylori pfr and sodB upstream areas. Studies of Fur-regulated genes in H. pylori have indicated that apo-Fur acts as a repressor, but our results demonstrate that iron-bound Fur activates (nifS) transcription.