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Unlike the case for other organisms, our previous report suggests a role for a non-base excision repair mechanism for the removal of 8-oxo-7,8-dihydroguanine (8-oxo-G) in\n            <jats:italic>P. gingivalis<\/jats:italic>\n            . Because the\n            <jats:italic>uvrB<\/jats:italic>\n            gene is known to be important in nucleotide excision repair, the role of this gene in the repair of oxidative stress-induced DNA damage was investigated. A 3.1-kb fragment containing the\n            <jats:italic>uvrB<\/jats:italic>\n            gene was PCR amplified from the chromosomal DNA of\n            <jats:italic>P. gingivalis<\/jats:italic>\n            W83. This gene was insertionally inactivated using the\n            <jats:italic>ermF-ermAM<\/jats:italic>\n            antibiotic cassette and used to create a\n            <jats:italic>uvrB<\/jats:italic>\n            -deficient mutant by allelic exchange. When plated on brucella blood agar, the mutant strain, designated\n            <jats:italic>P. gingivalis<\/jats:italic>\n            FLL144, was similar in black pigmentation and beta-hemolysis to the parent strain. In addition,\n            <jats:italic>P. gingivalis<\/jats:italic>\n            FLL144 demonstrated no significant difference in growth rate, proteolytic activity, or sensitivity to hydrogen peroxide from that of the parent strain. However, in contrast to the wild type,\n            <jats:italic>P. gingivalis<\/jats:italic>\n            FLL144 was significantly sensitive to UV irradiation. The enzymatic removal of 8-oxo-G from duplex DNA was unaffected by the inactivation of the\n            <jats:italic>uvrB<\/jats:italic>\n            gene. DNA affinity fractionation identified unique proteins that preferentially bound to the oligonucleotide fragment carrying the 8-oxo-G lesion. Collectively, these results suggest that the repair of oxidative stress-induced DNA damage involving 8-oxo-G may occur by a still undescribed mechanism in\n            <jats:italic>P. gingivalis<\/jats:italic>\n            .\n          <\/jats:p>","DOI":"10.1128\/jb.00919-08","type":"journal-article","created":{"date-parts":[[2008,10,11]],"date-time":"2008-10-11T00:45:11Z","timestamp":1223685911000},"page":"7985-7993","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":16,"title":["DNA Repair of 8-Oxo-7,8-Dihydroguanine Lesions in\n            <i>Porphyromonas gingivalis<\/i>"],"prefix":"10.1128","volume":"190","author":[{"given":"Leroy G.","family":"Henry","sequence":"first","affiliation":[{"name":"Division of Microbiology and Molecular Genetics"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lawrence","family":"Sandberg","sequence":"additional","affiliation":[{"name":"Division of Biochemistry, School of Medicine, Loma Linda University, Loma Linda, California 92350"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kangling","family":"Zhang","sequence":"additional","affiliation":[{"name":"Division of Biochemistry, School of Medicine, Loma Linda University, Loma Linda, California 92350"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hansel M.","family":"Fletcher","sequence":"additional","affiliation":[{"name":"Division of Microbiology and Molecular Genetics"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.69.1.325-335.2001"},{"key":"e_1_3_1_3_2","doi-asserted-by":"crossref","first-page":"40","DOI":"10.1034\/j.1399-302x.2000.150107.x","volume":"15","year":"2000","unstructured":"Abaibou, H., Q. 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