{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T23:58:56Z","timestamp":1789430336087,"version":"build-2803163510"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2008,1,1]],"date-time":"2008-01-01T00:00:00Z","timestamp":1199145600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    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.\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    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\n                    <jats:italic>recN<\/jats:italic>\n                    mutant strain of\n                    <jats:italic>H. pylori<\/jats:italic>\n                    was shown to be much more sensitive than its parent to mitomycin C, an agent predominantly causing DNA double-strand breaks. The\n                    <jats:italic>recN<\/jats:italic>\n                    strain was unable to survive exposure to either air or acid as well as the parent strain, and air exposure resulted in no viable\n                    <jats:italic>recN<\/jats:italic>\n                    cells recovered after 8 h. In oxidative stress conditions (i.e., air exposure), a\n                    <jats:italic>recN<\/jats:italic>\n                    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\n                    <jats:italic>H. pylori<\/jats:italic>\n                    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\n                    <jats:italic>recN<\/jats:italic>\n                    strain than for the wild type, indicating that RecN plays an important role in facilitating DNA recombination. In two separate mouse colonization experiments, the\n                    <jats:italic>recN<\/jats:italic>\n                    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\n                    <jats:italic>recN<\/jats:italic>\n                    strain by chromosomal insertion of a functional\n                    <jats:italic>recN<\/jats:italic>\n                    gene restored both the recombination frequency and mouse colonization ability to the wild-type levels. Thus,\n                    <jats:italic>H. pylori<\/jats:italic>\n                    RecN, as a component of DNA recombinational repair, plays a significant role in\n                    <jats:italic>H. pylori<\/jats:italic>\n                    survival in vivo.\n                  <\/jats:p>","DOI":"10.1128\/iai.00791-07","type":"journal-article","created":{"date-parts":[[2007,10,22]],"date-time":"2007-10-22T19:11:08Z","timestamp":1193080268000},"page":"153-160","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":37,"title":["Critical Role of RecN in Recombinational DNA Repair and Survival of\n                    <i>Helicobacter pylori<\/i>"],"prefix":"10.1128","volume":"76","author":[{"given":"Ge","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Microbiology, University of Georgia, Athens, Georgia 30602"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert J.","family":"Maier","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Georgia, Athens, Georgia 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