{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,16]],"date-time":"2025-07-16T11:56:40Z","timestamp":1752667000427},"reference-count":72,"publisher":"American Society for Microbiology","issue":"15","license":[{"start":{"date-parts":[[2005,8,1]],"date-time":"2005-08-01T00:00:00Z","timestamp":1122854400000},"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":[[2005,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            In\n            <jats:italic>Escherichia coli<\/jats:italic>\n            , PriA is central to the restart of chromosomal replication when replication fork progression is disrupted and is also involved in homologous recombination and DNA repair. To investigate the role of PriA in recombination and repair in\n            <jats:italic>Neisseria gonorrhoeae<\/jats:italic>\n            , we identified, cloned, and insertionally inactivated the gonococcal\n            <jats:italic>priA<\/jats:italic>\n            homologue. The\n            <jats:italic>priA<\/jats:italic>\n            mutant showed a growth deficiency and decreased DNA repair capability and was completely for deficient in DNA transformation compared to the isogenic parental strain. The\n            <jats:italic>priA<\/jats:italic>\n            mutant was also more sensitive to the oxidative damaging agents H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            and cumene hydroperoxide compared to the parental strain. These phenotypes were complemented by supplying a functional copy of\n            <jats:italic>priA<\/jats:italic>\n            elsewhere in the chromosome. The\n            <jats:italic>N. gonorrhoeae priA<\/jats:italic>\n            mutant showed no alteration in the frequency of pilin antigenic variation. We conclude that PriA participates in DNA repair and DNA transformation processes but not in pilin antigenic variation.\n          <\/jats:p>","DOI":"10.1128\/jb.187.15.5347-5355.2005","type":"journal-article","created":{"date-parts":[[2005,7,19]],"date-time":"2005-07-19T19:33:01Z","timestamp":1121801581000},"page":"5347-5355","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":45,"title":["Mutation of the\n            <i>priA<\/i>\n            Gene of\n            <i>Neisseria gonorrhoeae<\/i>\n            Affects DNA Transformation and DNA Repair"],"prefix":"10.1128","volume":"187","author":[{"given":"Kimberly A.","family":"Kline","sequence":"first","affiliation":[{"name":"Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H. Steven","family":"Seifert","sequence":"additional","affiliation":[{"name":"Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/jb.129.2.983-992.1977"},{"key":"e_1_3_2_3_2","doi-asserted-by":"crossref","first-page":"61","DOI":"10.1016\/S0378-1119(97)00653-7","volume":"208","year":"1998","unstructured":"Black, C. G., J. A. M. Fyfe, and J. K. Davies. 1998. Absence of an SOS-like system in Neisseria gonorrhoeae. 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