{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T02:07:33Z","timestamp":1792807653738,"version":"4.5.0"},"reference-count":49,"publisher":"National Academy of Sciences","issue":"27","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2010,7,6]]},"abstract":"<jats:p>\n                    The\n                    <jats:italic>Enterococcus faecalis<\/jats:italic>\n                    pathogenicity island (PAI) encodes known virulence traits and &gt;100 additional genes with unknown roles in enterococcal biology. Phage-related integration and excision genes, and direct repeats flanking the island, suggest it moves as an integrative conjugative element (ICE). However, transfer was observed not to require these genes. Transfer only occurred from donors possessing a pheromone responsive-type of conjugative plasmid, and was invariably accompanied by transfer of flanking donor chromosome sequences. Deletion of plasmid transfer functions, including the\n                    <jats:italic>cis<\/jats:italic>\n                    -acting origin of transfer (\n                    <jats:italic>oriT<\/jats:italic>\n                    ), abolished movement. In addition to demonstrating PAI movement by a mechanism involving plasmid integration, we observed transfer of a selectable marker placed virtually anywhere on the chromosome. Transfer of this selectable marker was observed to be accompanied by chromosome-chromosome transfer of vancomycin resistance, MLST markers, and capsule genes as well. Plasmid mobilization therefore appears to be a major mechanism for horizontal gene transfer in the evolution of antibiotic resistant\n                    <jats:italic>E. faecalis<\/jats:italic>\n                    strains capable of causing human infection.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1000139107","type":"journal-article","created":{"date-parts":[[2010,6,21]],"date-time":"2010-06-21T22:44:55Z","timestamp":1277160295000},"page":"12269-12274","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":186,"title":["Mechanism of chromosomal transfer of\n                    <i>Enterococcus faecalis<\/i>\n                    pathogenicity island, capsule, antimicrobial resistance, and other traits"],"prefix":"10.1073","volume":"107","author":[{"given":"Janet M.","family":"Manson","sequence":"first","affiliation":[{"name":"Departments of aOphthalmology and"},{"name":"Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lynn E.","family":"Hancock","sequence":"additional","affiliation":[{"name":"Division of Biology, Kansas State University, Manhattan, KS 66506"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael S.","family":"Gilmore","sequence":"additional","affiliation":[{"name":"Departments of aOphthalmology and"},{"name":"Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2010,6,4]]},"reference":[{"key":"e_1_3_3_1_2","first-page":"149","article-title":"The emergence of enterococci as a cause of nosocomial infection","volume":"55","author":"Hunt CP","year":"1998","unstructured":"CP Hunt, The emergence of enterococci as a cause of nosocomial infection. 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