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The high pathogenicity of\n \n S<\/jats:italic>\n <\/jats:styled-content>\n .\u2009suis<\/jats:italic>\n may be due in part to a laterally acquired pathogenicity island (renamed\n SsPI<\/jats:styled-content>\n \u20101), which can spontaneously excise and transfer to recipients. Cells harboring excised\n SsPI<\/jats:styled-content>\n \u20101 can potentially lose this island if cell division occurs prior to its reintegration; however, attempts to cure\n SsPI<\/jats:styled-content>\n \u20101 from the host cells have been unsuccessful. Here, we report that an\n SsPI<\/jats:styled-content>\n \u20101\u2010borne\n E<\/jats:styled-content>\n psilon\/\n Z<\/jats:styled-content>\n eta toxin\u2013antitoxin system (designated\n SezAT<\/jats:styled-content>\n ) promotes\n SsPI<\/jats:styled-content>\n \u20101 stability in bacterial populations. The\n sez<\/jats:italic>\n \n AT<\/jats:italic>\n <\/jats:styled-content>\n locus consists of two closely linked\n sez<\/jats:italic>\n \n T<\/jats:italic>\n <\/jats:styled-content>\n and\n sez<\/jats:italic>\n \n A<\/jats:italic>\n <\/jats:styled-content>\n genes encoding a toxin and its cognate antitoxin, respectively. Overproduction of\n SezT<\/jats:styled-content>\n induces a bactericidal effect that can be neutralized by co\u2010expression of\n SezA<\/jats:styled-content>\n , but not by its later action. When devoid of a functional\n SezAT<\/jats:styled-content>\n system, large\u2010scale deletion of\n SsPI<\/jats:styled-content>\n \u20101 is straightforward. Thus,\n SezAT<\/jats:styled-content>\n serves to ensure inheritance of\n SsPI<\/jats:styled-content>\n \u20101 during cell division, which may explain the persistence of epidemic\n \n S<\/jats:italic>\n <\/jats:styled-content>\n .\u2009suis<\/jats:italic>\n . This report presents the first functional characterization of\n TA<\/jats:styled-content>\n loci in\n \n S<\/jats:italic>\n <\/jats:styled-content>\n .\u2009suis<\/jats:italic>\n , and the first biochemical evidence for the adaptive significance of the\n E<\/jats:styled-content>\n psilon\/\n Z<\/jats:styled-content>\n eta system in the evolution of pathogen virulence.\n <\/jats:p>","DOI":"10.1111\/mmi.13116","type":"journal-article","created":{"date-parts":[[2015,7,3]],"date-time":"2015-07-03T12:06:45Z","timestamp":1435925205000},"page":"243-257","source":"Crossref","is-referenced-by-count":38,"title":["The chromosomal\n SezAT<\/scp>\n toxin\u2013antitoxin system promotes the maintenance of the\n SsPI<\/scp>\n \u20101 pathogenicity island in epidemic\n \n S<\/i>\n <\/scp>\n treptococcus suis<\/i>"],"prefix":"10.1111","volume":"98","author":[{"given":"Xinyue","family":"Yao","sequence":"first","affiliation":[{"name":"Department of Microbiology Third Military Medical University Chongqing 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