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In our studies of the major pathogen and model organism<jats:italic>Neisseria meningitidis<\/jats:italic>, we constructed a panel of mutants inactivating genes involved in base excision repair, mismatch repair, nucleotide excision repair (NER), translesion synthesis, and recombinational repair pathways. The highest spontaneous mutation frequency among the<jats:italic>N. meningitidis<\/jats:italic>single mutants was found in the MutY-deficient strain as opposed to<jats:italic>mutS<\/jats:italic>mutants in<jats:italic>Escherichia coli<\/jats:italic>, indicating a role for meningococcal MutY in antibiotic resistance development. Recombinational repair was recognized as a major pathway counteracting methyl methanesulfonate-induced alkylation damage in the<jats:italic>N. meningitidis<\/jats:italic>. In contrast to what has been shown in other species, meningococcal NER did not contribute significantly to repair of alkylation-induced DNA damage, and meningococcal recombinational repair may thus be one of the main pathways for removal of abasic (apurinic\/apyrimidinic) sites and strand breaks in DNA. Conversely, NER was identified as the main meningococcal defense pathway against UV-induced DNA damage.<jats:italic>N. meningitidis<\/jats:italic>RecA single mutants exhibited only a moderate decrease in survival after UV exposure as opposed to<jats:italic>E. coli recA<\/jats:italic>strains, which are extremely UV sensitive, possibly reflecting the lack of a meningococcal SOS response. In conclusion, distinct differences between<jats:italic>N. meningitidis<\/jats:italic>and established DNA repair characteristics in<jats:italic>E. coli<\/jats:italic>and other species were identified.<\/jats:p>","DOI":"10.1128\/jb.00161-07","type":"journal-article","created":{"date-parts":[[2007,5,19]],"date-time":"2007-05-19T14:27:13Z","timestamp":1179584833000},"page":"5728-5737","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":33,"title":["Genetic Interactions of DNA Repair Pathways in the Pathogen<i>Neisseria meningitidis<\/i>"],"prefix":"10.1128","volume":"189","author":[{"given":"Tonje","family":"Davidsen","sequence":"first","affiliation":[{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo"},{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, Rikshospitalet-Radiumhospitalet Medical Centre, Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hanne K.","family":"Tuven","sequence":"additional","affiliation":[{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Magnar","family":"Bj\u00f8ra\u030as","sequence":"additional","affiliation":[{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Einar A.","family":"R\u00f8dland","sequence":"additional","affiliation":[{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tone","family":"T\u00f8njum","sequence":"additional","affiliation":[{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo"},{"name":"Centre for Molecular Biology and Neuroscience and Institute of Microbiology, Rikshospitalet-Radiumhospitalet Medical Centre, Oslo, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"1123","DOI":"10.1093\/nar\/gki259","volume":"33","year":"2005","unstructured":"Alseth, I., F. 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