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Infection and Immunity, October 2005, p. 6437-6445, Vol. 73, No. 10
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.10.6437-6445.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Acid-Induced Activation of the Urease Promoters Is Mediated Directly by the ArsRS Two-Component System of Helicobacter pylori

Michael Pflock,1,{dagger} Simone Kennard,1,{dagger} Isabel Delany,2 Vincenzo Scarlato,2 and Dagmar Beier1*

Theodor-Boveri-Institut für Biowissenschaften, Lehrstuhl für Mikrobiologie, Universität Würzburg, Am Hubland, D-97074 Würzburg, Germany,1 Molecular Immunology Unit, Chiron Vaccines, Via Fiorentina 1, 53100 Siena, Italy2

Received 17 March 2005/ Returned for modification 22 May 2005/ Accepted 25 May 2005

The nickel-containing enzyme urease is an essential colonization factor of the human gastric pathogen Helicobacter pylori which enables the bacteria to survive the low-pH conditions of the stomach. Transcription of the urease genes is positively controlled in response to increasing concentrations of nickel ions and acidic pH. Here we demonstrate that acid-induced transcription of the urease genes is mediated directly by the ArsRS two-component system. Footprint analyses identify binding sites of the phosphorylated ArsR response regulator within the ureA and ureI promoters. Furthermore, deletion of a distal upstream ArsR binding site of the ureA promoter demonstrates its role in acid-dependent activation of the promoter. In addition, acid-induced transcription of the ureA gene is unaltered in a nikR mutant, providing evidence that pH-responsive regulation and nickel-responsive regulation of the ureA promoter are mediated by independent mechanisms involving the ArsR response regulator and the NikR protein.

* Corresponding author. Mailing address: Theodor-Boveri-Institut für Biowissenschaften, Lehrstuhl für Mikrobiologie, Universität Würzburg, Am Hubland, 97074 Würzburg, Germany. Phone: 49931-8884421. Fax: 49-931-8884402. E-mail: d.beier{at}biozentrum.uni-wuerzburg.de.

Editor: V. J. DiRita

{dagger} These authors contributed equally to the present study.

Infection and Immunity, October 2005, p. 6437-6445, Vol. 73, No. 10
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.10.6437-6445.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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