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Infection and Immunity, January 2009, p. 286-291, Vol. 77, No. 1
0019-9567/09/$08.00+0 doi:10.1128/IAI.00970-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Microbiology, University of Georgia, Athens, Georgia 30602
Received 1 August 2008/ Returned for modification 2 September 2008/ Accepted 23 October 2008
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-stranded (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 WT 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 h 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.
Published ahead of print on 3 November 2008.
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