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UvrD Helicase Suppresses Recombination and DNA Damage-Induced Deletions

Departments of Microbiology and Medicine, New York University School of Medicine, and VA Medical Center, New York, New York

Received 21 February 2006/ Accepted 21 May 2006

UvrD, a highly conserved helicase involved in mismatch repair, nucleotide excision repair (NER), and recombinational repair, plays a critical role in maintaining genomic stability and facilitating DNA lesion repair in many prokaryotic species. In this report, we focus on the UvrD homolog in Helicobacter pylori, a genetically diverse organism that lacks many known DNA repair proteins, including those involved in mismatch repair and recombinational repair, and that is noted for high levels of inter- and intragenomic recombination and mutation. H. pylori contains numerous DNA repeats in its compact genome and inhabits an environment rich in DNA-damaging agents that can lead to increased rearrangements between such repeats. We find that H. pylori UvrD functions to repair DNA damage and limit homologous recombination and DNA damage-induced genomic rearrangements between DNA repeats. Our results suggest that UvrD and other NER pathway proteins play a prominent role in maintaining genome integrity, especially after DNA damage; thus, NER may be especially critical in organisms such as H. pylori that face high-level genotoxic stress in vivo.

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This article has been cited by other articles:

• Kang, J., Blaser, M. J. (2008). Repair and Antirepair DNA Helicases in Helicobacter pylori. J. Bacteriol. 190: 4218-4224 [Abstract] [Full Text]  
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