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Infect. Immun. doi:10.1128/IAI.00791-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Recombinational DNA repair and survival of Helicobacter pylori: Critical role of RecN

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

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

	Abstract

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 (pre-synapsis) 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 either to air or acid as well as the parent strain, with air exposure resulting in no viable recN cells recovered after 8 hours. 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 ability of strains, their transformation ability was compared by separately monitoring transformation using H. pylori DNA fragments containing either a site-specific mutation (conferring rifampicin resistance) or a large insertion (kanamycin resistance cassette). The transformation frequency using the two types of DNA donor was, respectively, 10- and 50-fold lower for the recN strain than for the wild type, indicating 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 number of recovered cells averaged 10-fold less for the mutant compared to 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 level. Thus H. pylori RecN, as a component of DNA recombinational repair, plays a significant role for H. pylori survival in vivo.