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Journal of Bacteriology, May 2006, p. 3449-3462, Vol. 188, No. 10
0021-9193/06/$08.00+0     doi:10.1128/JB.188.10.3449-3462.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Characterization of the ArsRS Regulon of Helicobacter pylori, Involved in Acid Adaptation{dagger}

Michael Pflock,1,{ddagger} Nadja Finsterer,1,{ddagger} Biju Joseph,1 Hans Mollenkopf,2 Thomas F. Meyer,3 and Dagmar Beier1*

Theodor-Boveri-Institut für Biowissenschaften, Lehrstuhl für Mikrobiologie, Universität Würzburg, Am Hubland, D-97074 Würzburg,1 Max-Planck-Institut für Infektionsbiologie, Microarray Core Facility,2 Abteilung Molekulare Biologie, Schumannstrasse 21/22, D-10117 Berlin, Germany3

Received 17 January 2006/ Accepted 27 February 2006

The human gastric pathogen Helicobacter pylori is extremely well adapted to the highly acidic conditions encountered in the stomach. The pronounced acid resistance of H. pylori relies mainly on the ammonia-producing enzyme urease; however, urease-independent mechanisms are likely to contribute to acid adaptation. Acid-responsive gene regulation is mediated at least in part by the ArsRS two-component system consisting of the essential OmpR-like response regulator ArsR and the nonessential cognate histidine kinase ArsS, whose autophosphorylation is triggered in response to low pH. In this study, by global transcriptional profiling of an ArsS-deficient H. pylori mutant grown at pH 5.0, we define the ArsR~P-dependent regulon consisting of 109 genes, including the urease gene cluster, the genes encoding the aliphatic amidases AmiE and AmiF, and the rocF gene encoding arginase. We show that ArsR~P controls the acid-induced transcription of amiE and amiF by binding to extended regions located upstream of the –10 box of the respective promoters. In contrast, transcription of rocF is repressed by ArsR~P at neutral, acidic, and mildly alkaline pH via high-affinity binding of the response regulator to a site overlapping the promoter of the rocF gene.

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

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

{ddagger} Both authors contributed equally to the present study.

Journal of Bacteriology, May 2006, p. 3449-3462, Vol. 188, No. 10
0021-9193/06/$08.00+0     doi:10.1128/JB.188.10.3449-3462.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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