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Journal of Bacteriology, June 2005, p. 3708-3712, Vol. 187, No. 11
0021-9193/05/$08.00+0     doi:10.1128/JB.187.11.3708-3712.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

16S rRNA Mutations That Confer Tetracycline Resistance in Helicobacter pylori Decrease Drug Binding in Escherichia coli Ribosomes

Lisa Nonaka,1,{dagger} Sean R. Connell,3 and Diane E. Taylor1,2*

Department of Medical Microbiology and Immunology,1 Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada,2 Institut für Medizinische Physik und Biophysik, Universitätsklinikum Charite, Berlin, Germany3

Received 5 November 2004/ Accepted 25 February 2005

Tetracycline resistance in clinical isolates of Helicobacter pylori has been associated with nucleotide substitutions at positions 965 to 967 in the 16S rRNA. We constructed mutants which had different sequences at 965 to 967 in the 16S rRNA gene present on a multicopy plasmid in Escherichia coli strain TA527, in which all seven rrn genes were deleted. The MICs for tetracycline of all mutants having single, double, or triple substitutions at the 965 to 967 region that were previously found in highly resistant H. pylori isolates were higher than that of the mutant exhibiting the wild-type sequence of tetracycline-susceptible H. pylori. The MIC of the mutant with the 965TTC967 triple substitution was 32 times higher than that of the E. coli mutant with the 965AGA967 substitution present in wild-type H. pylori. The ribosomes extracted from the tetracycline-resistant E. coli 965TTC967 variant bound less tetracycline than E. coli with the wild-type H. pylori sequence at this region. The concentration of tetracycline bound to the ribosome was 40% that of the wild type. The results of this study suggest that tetracycline binding to the primary binding site (Tet-1) of the ribosome at positions 965 to 967 is influenced by its sequence patterns, which form the primary binding site for tetracycline.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, 1-28 Medical Sciences Building, University of Alberta, Edmonton, Alberta T6G 2H7, Canada. Phone: (780) 492-4777. Fax: (780) 492-7521. E-mail: diane.taylor{at}ualberta.ca.

{dagger} Present address: Center for Marine Environmental Studies, Ehime University, 3 Bunkyo-cho, Matsuyama 790-8577, Japan.

Journal of Bacteriology, June 2005, p. 3708-3712, Vol. 187, No. 11
0021-9193/05/$08.00+0     doi:10.1128/JB.187.11.3708-3712.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Anoushiravani, M., Falsafi, T., Niknam, V. (2009). Proton motive force-dependent efflux of tetracycline in clinical isolates of Helicobacter pylori. J Med Microbiol 58: 1309-1313 [Abstract] [Full Text]  
  • Megraud, F., Lehours, P. (2007). Helicobacter pylori Detection and Antimicrobial Susceptibility Testing. Clin. Microbiol. Rev. 20: 280-322 [Abstract] [Full Text]  


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