Previous Article | Next Article ![]()
Journal of Bacteriology, August 2006, p. 5450-5459, Vol. 188, No. 15
0021-9193/06/$08.00+0 doi:10.1128/JB.00275-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
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.
Supplemental material for this article may be found at http://jb.asm.org/.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»