IAI Accepts, published online ahead of print on 3 November 2008

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Infect. Immun. doi:10.1128/IAI.00970-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

A RecB-like helicase in Helicobacter pylori is important for DNA repair and host colonization

Ge Wang and Robert J. Maier^*

Department of Microbiology, University of Georgia, Athens, Georgia 30602

^* To whom correspondence should be addressed. Email: rmaier{at}uga.edu.

The human gastric pathogen Helicobacter pylori encounters frequent oxidative and acid stress in its specific niche, and this causes bacterial DNA damage. H. pylori exhibits a very high degree of DNA recombination which is required for repairing both DNA double strand (ds) breaks and blocked replication forks. Nevertheless, few genes encoding components of DNA recombinational repair processes have been identified in H. pylori. An H. pylori mutant defective in a putative helicase gene (HP1553) was constructed and characterized herein. The HP1553 mutant strain was much more sensitive to mitomycin C than the wild type strain, indicating that HP1553 is required for repair of DNA ds breaks. Disruption of HP1553 resulted in a significant decrease in the DNA recombination frequency, suggesting that HP1553 is involved in DNA recombination processes, probably functioning as a RecB-like helicase. HP1553 was shown to be important for H. pylori protection against oxidative stress-induced DNA damage, as the exposure of the HP1553 mutant cells to air for 6 hours caused significant fragmentation of genomic DNA and led to cell death. In a mouse infection model, the HP1553 mutant strain displayed a greatly reduced ability to colonize the host stomachs, indicating that HP1553 plays a significant role in H. pylori survival/colonization in the host.

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• Cromie, G. A. (2009). Phylogenetic Ubiquity and Shuffling of the Bacterial RecBCD and AddAB Recombination Complexes. J. Bacteriol. 191: 5076-5084 [Abstract] [Full Text]