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Journal of Bacteriology, April 2009, p. 2405-2408, Vol. 191, No. 7
0021-9193/09/$08.00+0     doi:10.1128/JB.01657-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

An Intact Urease Assembly Pathway Is Required To Compete with NikR for Nickel Ions in Helicobacter pylori{triangledown} ,{dagger}

Erin L. Benanti and Peter T. Chivers*

Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, Missouri 63110

Received 21 November 2008/ Accepted 10 January 2009

We examined the effects of urease and hydrogenase assembly gene deletions on NikR activation in H. pylori strains 26695 and G27. The loss of any component of urease assembly increased NikR activity under Ni2+-limiting conditions, as measured by reduced transcript levels and 63Ni accumulation. Additionally, SlyD functioned in urease assembly in strain 26695.

* Corresponding author. Mailing address: Department of Biochemistry and Molecular Biophysics, Box 8231, Washington University School of Medicine, 660 S. Euclid Ave. St. Louis, MO 63110. Phone: (314) 362-1496. Fax: (314) 362-7183. E-mail: chivers{at}wustl.edu

{triangledown} Published ahead of print on 23 January 2009.

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

Journal of Bacteriology, April 2009, p. 2405-2408, Vol. 191, No. 7
0021-9193/09/$08.00+0     doi:10.1128/JB.01657-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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