{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T01:21:16Z","timestamp":1790904076343,"version":"4.1.0"},"reference-count":33,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2006,2,15]],"date-time":"2006-02-15T00:00:00Z","timestamp":1139961600000},"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":["J Bacteriol"],"published-print":{"date-parts":[[2006,2,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Exonuclease III, encoded by the\n            <jats:italic>xthA<\/jats:italic>\n            gene, plays a central role in the base excision pathway of DNA repair in bacteria. Studies with\n            <jats:italic>Escherichia coli xthA<\/jats:italic>\n            mutants have also shown that exonuclease III participates in the repair of oxidative damage to DNA. An isogenic\n            <jats:italic>xthA-1<\/jats:italic>\n            mutant (designated CAM220) derived from virulent\n            <jats:italic>Brucella abortus<\/jats:italic>\n            2308 exhibited increased sensitivity to the alkylating agent methyl methanesulfonate (MMS) compared to the parent strain. In contrast, 2308 and the isogenic\n            <jats:italic>xthA-1<\/jats:italic>\n            mutant displayed similar levels of resistance to the DNA cross-linker mitomycin C. These phenotypic properties are those that would be predicted for a strain defective in base excision repair. The\n            <jats:italic>B. abortus xthA-1<\/jats:italic>\n            mutant also displayed reduced resistance to killing by H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            and the ONOO\n            <jats:sup>\u2212<\/jats:sup>\n            -generating compound 3-morpholinosydnonimine (SIN-1) compared to strain 2308, indicating that the\n            <jats:italic>xthA-1<\/jats:italic>\n            gene product participates in protecting\n            <jats:italic>B. abortus<\/jats:italic>\n            2308 from oxidative damage. Introducing a plasmid-borne copy of the parental\n            <jats:italic>xthA-1<\/jats:italic>\n            gene into CAM220 restored wild-type resistance of this mutant to MMS, H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            , and SIN-1. Although the\n            <jats:italic>B. abortus xthA-1<\/jats:italic>\n            mutant exhibited increased sensitivity to oxidative killing compared to the parental strain in laboratory assays, CAM220 and 2308 displayed equivalent spleen colonization profiles in BALB\/c mice through 8 weeks postinfection and equivalent intracellular survival and replication profiles in cultured murine macrophages. Thus, although the\n            <jats:italic>xthA-1<\/jats:italic>\n            gene product participates in base excision repair and resistance to oxidative killing in\n            <jats:italic>B. abortus<\/jats:italic>\n            2308, XthA-1 is not required for wild-type virulence of this strain in the mouse model.\n          <\/jats:p>","DOI":"10.1128\/jb.188.4.1295-1300.2006","type":"journal-article","created":{"date-parts":[[2006,2,1]],"date-time":"2006-02-01T19:40:30Z","timestamp":1138822830000},"page":"1295-1300","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":21,"title":["The\n            <i>Brucella abortus xthA-1<\/i>\n            Gene Product Participates in Base Excision Repair and Resistance to Oxidative Killing but Is Not Required for Wild-Type Virulence in the Mouse Model"],"prefix":"10.1128","volume":"188","author":[{"given":"Michael L.","family":"Hornback","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, North Carolina 27834"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"II","given":"R. Martin","family":"Roop","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, North Carolina 27834"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"1047","DOI":"10.1172\/JCI117750","volume":"95","year":"1995","unstructured":"Buchmeier, N. A., S. J. Libby, Y. Xu, P. C. Loewen, J. Switala, D. G. Guiney, and F. C. Fang. 1995. DNA repair is more important than catalase for Salmonella virulence in mice. J. Clin. Investig.95:1047-1053.","journal-title":"J. Clin. Investig."},{"key":"e_1_3_2_3_2","doi-asserted-by":"crossref","first-page":"25978","DOI":"10.1016\/S0021-9258(18)47147-5","volume":"269","year":"1994","unstructured":"Burger, R. M., K. Drlica, and B. Birdsall. 1994. The DNA cleavage pathway of iron bleomycin. Strand scission precedes deoxyribose 3-phosphate bond cleavage. J. Biol. 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