{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T13:59:06Z","timestamp":1761919146657},"reference-count":61,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2008,9,1]],"date-time":"2008-09-01T00:00:00Z","timestamp":1220227200000},"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":["Infect Immun"],"published-print":{"date-parts":[[2008,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            RecA is a key protein linking genetic recombination to DNA replication and repair in bacteria. Previous functional characterization of\n            <jats:italic>Borrelia burgdorferi<\/jats:italic>\n            RecA indicated that the protein is mainly involved in genetic recombination rather than DNA repair. Genetic recombination may play a role in\n            <jats:italic>B. burgdorferi<\/jats:italic>\n            persistence by generation of antigenic variation. We report here the isolation of a\n            <jats:italic>recA<\/jats:italic>\n            null mutant in an infectious\n            <jats:italic>B. burgdorferi<\/jats:italic>\n            strain. Comparison of the in vitro growth characteristics of the mutant with those of the wild-type strain under various conditions showed no significant differences. While the RecA mutant was moderately more sensitive to UV irradiation and mitomycin C than the wild-type strain, the lack of RecA abolished allelic exchange in the mutant. Absence of RecA did not affect the ability of the mutant to infect mice. However, the RecA mutant was attenuated for joint infection in competitive-infection assays with the wild-type strain.\n            <jats:italic>vlsE<\/jats:italic>\n            sequence variation in mice was observed in both wild-type and RecA mutant spirochetes, indicating that the mechanism of antigenic variation is not homologous genetic recombination.\n          <\/jats:p>","DOI":"10.1128\/iai.00027-08","type":"journal-article","created":{"date-parts":[[2008,7,8]],"date-time":"2008-07-08T00:34:50Z","timestamp":1215477290000},"page":"4009-4018","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":32,"title":["<i>Borrelia burgdorferi vlsE<\/i>\n            Antigenic Variation Is Not Mediated by RecA"],"prefix":"10.1128","volume":"76","author":[{"given":"Dionysios","family":"Liveris","sequence":"first","affiliation":[{"name":"Department of Microbiology &amp; Immunology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vishwaroop","family":"Mulay","sequence":"additional","affiliation":[{"name":"Department of Biochemistry &amp; Molecular Biology, New York Medical College, Valhalla, New York 10595"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sabina","family":"Sandigursky","sequence":"additional","affiliation":[{"name":"Department of Microbiology &amp; Immunology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ira","family":"Schwartz","sequence":"additional","affiliation":[{"name":"Department of Microbiology &amp; Immunology"},{"name":"Department of Biochemistry &amp; Molecular Biology, New York Medical College, Valhalla, New York 10595"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/27.5.1223"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2007.05895.x"},{"key":"e_1_3_2_4_2","first-page":"959","volume":"143","year":"1993","unstructured":"Barthold, S. 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