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The DNA glycosylase MutY of the base excision repair pathway is involved in the protection against oxidative stress. MC MutY expressed in\n            <jats:italic>Escherichia coli<\/jats:italic>\n            exhibited base excision activity towards DNA substrates containing A:7,8-dihydro-8-oxo-2\u2032-deoxyguanosine and A:C mismatches. Expression in\n            <jats:italic>E. coli<\/jats:italic>\n            fully suppressed the elevated spontaneous mutation rate found in the\n            <jats:italic>E. coli mutY<\/jats:italic>\n            mutant. An assessment of MutY activity in lysates of neisserial wild-type and\n            <jats:italic>mutY<\/jats:italic>\n            mutant strains showed that both MC and gonococcal (GC) MutY is expressed and active in vivo. Strikingly, MC and GC\n            <jats:italic>mutY<\/jats:italic>\n            mutants exhibited 60- to 140-fold and 20-fold increases in mutation rates, respectively, compared to the wild-type strains. Moreover, the differences in transitions and transversions in\n            <jats:italic>rpoB<\/jats:italic>\n            conferring rifampin resistance observed with the wild type and mutants demonstrated that the neisserial MutY enzyme works in preventing GC\u2192AT transversions. These findings are important in the context of models linking mutator phenotypes of disease isolates to microbial fitness.\n          <\/jats:p>","DOI":"10.1128\/jb.187.8.2801-2809.2005","type":"journal-article","created":{"date-parts":[[2005,4,1]],"date-time":"2005-04-01T22:33:42Z","timestamp":1112394822000},"page":"2801-2809","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":34,"title":["Antimutator Role of DNA Glycosylase MutY in Pathogenic\n            <i>Neisseria<\/i>\n            Species"],"prefix":"10.1128","volume":"187","author":[{"given":"T.","family":"Davidsen","sequence":"first","affiliation":[{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo, Rikshospitalet, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Bj\u00f8ra\u030as","sequence":"additional","affiliation":[{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo, Rikshospitalet, Oslo, Norway"},{"name":"Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. C.","family":"Seeberg","sequence":"additional","affiliation":[{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo, Rikshospitalet, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"T\u00f8njum","sequence":"additional","affiliation":[{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo, Rikshospitalet, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"2787","DOI":"10.1093\/nar\/15.7.2787","volume":"15","year":"1987","unstructured":"Bjelland, S., and E. Seeberg. 1987. 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