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Journal of Bacteriology, June 2005, p. 3687-3692, Vol. 187, No. 11
0021-9193/05/$08.00+0     doi:10.1128/JB.187.11.3687-3692.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Iron-Responsive Regulation of the Helicobacter pylori Iron-Cofactored Superoxide Dismutase SodB Is Mediated by Fur

Florian D. Ernst,1,2,3 Georg Homuth,3,{dagger} Jeroen Stoof,1 Ulrike Mäder,3,{dagger} Barbara Waidner,2 Ernst J. Kuipers,1 Manfred Kist,2 Johannes G. Kusters,1 Stefan Bereswill,2,{ddagger} and Arnoud H. M. van Vliet1*

Department of Gastroenterology and Hepatology, Erasmus MC-University Medical Center, Rotterdam, The Netherlands,1 Department of Microbiology and Hygiene, Institute of Medical Microbiology and Hygiene, University Hospital of Freiburg, Freiburg, Germany,2 Institut für Mikrobiologie und Molekularbiologie, Ernst-Moritz-Arndt-Universität Greifswald, Greifswald, Germany3

Received 18 September 2004/ Accepted 16 February 2005

Maintaining iron homeostasis is a necessity for all living organisms, as free iron augments the generation of reactive oxygen species like superoxide anions, at the risk of subsequent lethal cellular damage. The iron-responsive regulator Fur controls iron metabolism in many bacteria, including the important human pathogen Helicobacter pylori, and thus is directly or indirectly involved in regulation of oxidative stress defense. Here we demonstrate that Fur is a direct regulator of the H. pylori iron-cofactored superoxide dismutase SodB, which is essential for the defense against toxic superoxide radicals. Transcription of the sodB gene was iron induced in H. pylori wild-type strain 26695, resulting in expression of the SodB protein in iron-replete conditions but an absence of expression in iron-restricted conditions. Mutation of the fur gene resulted in constitutive, iron-independent expression of SodB. Recombinant H. pylori Fur protein bound with low affinity to the sodB promoter region, but addition of the iron substitute Mn2+ abolished binding. The operator sequence of the iron-free form of Fur, as identified by DNase I footprinting, was located directly upstream of the sodB gene at positions –5 to –47 from the transcription start site. The direct role of Fur in regulation of the H. pylori sodB gene contrasts with the small-RNA-mediated sodB regulation observed in Escherichia coli. In conclusion, H. pylori Fur is a versatile regulator involved in many pathways essential for gastric colonization, including superoxide stress defense.

* Corresponding author. Mailing address: Department of Gastroenterology and Hepatology, Erasmus MC-University Medical Center, Dijkzigt L-4, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. Phone: 31-10-463-5944. Fax: 31-10-463-2793. E-mail: a.h.m.vanvliet{at}erasmusmc.nl.

{dagger} Present address: School of Cell and Molecular Biosciences, Newcastle University Medical School, Newcastle-upon-Tyne, United Kingdom.

{ddagger} Present address: Institut für Mikrobiologie und Hygiene, Campus Charité Mitte, Berlin, Germany.

Journal of Bacteriology, June 2005, p. 3687-3692, Vol. 187, No. 11
0021-9193/05/$08.00+0     doi:10.1128/JB.187.11.3687-3692.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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