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Infection and Immunity, January 2008, p. 153-160, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.00791-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Critical Role of RecN in Recombinational DNA Repair and Survival of Helicobacter pylori

Ge Wang and Robert J. Maier^*

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

Received 10 June 2007/ Returned for modification 20 July 2007/ Accepted 10 October 2007

Homologous recombination is one of the key mechanisms responsible for the repair of DNA double-strand breaks. Recombinational repair normally requires a battery of proteins, each with specific DNA recognition, strand transfer, resolution, or other functions. Helicobacter pylori lacks many of the proteins normally involved in the early stage (presynapsis) of recombinational repair, but it has a RecN homologue with an unclear function. A recN mutant strain of H. pylori was shown to be much more sensitive than its parent to mitomycin C, an agent predominantly causing DNA double-strand breaks. The recN strain was unable to survive exposure to either air or acid as well as the parent strain, and air exposure resulted in no viable recN cells recovered after 8 h. In oxidative stress conditions (i.e., air exposure), a recN strain accumulated significantly more damaged (multiply fragmented) DNA than the parent strain. To assess the DNA recombination abilities of strains, their transformation abilities were compared by separately monitoring transformation using H. pylori DNA fragments containing either a site-specific mutation (conferring rifampin resistance) or a large insertion (kanamycin resistance cassette). The transformation frequencies using the two types of DNA donor were 10- and 50-fold lower, respectively, for the recN strain than for the wild type, indicating that RecN plays an important role in facilitating DNA recombination. In two separate mouse colonization experiments, the recN strain colonized most of the stomachs, but the average number of recovered cells was 10-fold less for the mutant than for the parent strain (a statistically significant difference). Complementation of the recN strain by chromosomal insertion of a functional recN gene restored both the recombination frequency and mouse colonization ability to the wild-type levels. Thus, H. pylori RecN, as a component of DNA recombinational repair, plays a significant role in H. pylori survival in vivo.

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* Corresponding author. Mailing address: Department of Microbiology, 815 Biological Sciences Building, University of Georgia, Athens, GA 30602. Phone: (706) 542-2323. Fax: (706) 542-2674. E-mail: rmaier{at}uga.edu

Published ahead of print on 22 October 2007.

Editor: A. Camilli

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Infection and Immunity, January 2008, p. 153-160, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.00791-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

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