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Many Gram-positive bacteria, including the human pathogen\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Listeria monocytogenes<\/jats:named-content>\n            , possess an additional nonessential specialized ATPase, SecA2. SecA2-dependent secretion is required for normal cell morphology and virulence in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">L. monocytogenes<\/jats:named-content>\n            ; however, the mechanism of export via this pathway is poorly understood.\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">L. monocytogenes<\/jats:named-content>\n            <jats:italic>secA2<\/jats:italic>\n            mutants form rough colonies, have septation defects, are impaired for swarming motility, and form small plaques in tissue culture cells. In this study, 70 spontaneous mutants were isolated that restored swarming motility to\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">L. monocytogenes<\/jats:named-content>\n            <jats:italic>secA2<\/jats:italic>\n            mutants. Most of the mutants had smooth colony morphology and septated normally, but all were lysozyme sensitive. Five representative mutants were subjected to whole-genome sequencing. Four of the five had mutations in proteins encoded by the\n            <jats:italic>lmo2769<\/jats:italic>\n            operon that conferred lysozyme sensitivity and increased swarming but did not rescue virulence defects. A point mutation in\n            <jats:italic>secY<\/jats:italic>\n            was identified that conferred smooth colony morphology to\n            <jats:italic>secA2<\/jats:italic>\n            mutants, restored wild-type plaque formation, and increased virulence in mice. This\n            <jats:italic>secY<\/jats:italic>\n            mutation resembled a\n            <jats:italic>prl<\/jats:italic>\n            suppressor known to expand the repertoire of proteins secreted through the SecY translocation complex. Accordingly, the \u0394\n            <jats:italic>secA2prlA1<\/jats:italic>\n            mutant showed wild-type secretion levels of P60, an established SecA2-dependent secreted autolysin. Although the\n            <jats:italic>prl<\/jats:italic>\n            mutation largely suppressed almost all of the measurable SecA2-dependent traits, the \u0394\n            <jats:italic>secA2prlA1<\/jats:italic>\n            mutant was still less virulent\n            <jats:italic>in vivo<\/jats:italic>\n            than the wild-type strain, suggesting that SecA2 function was still required for pathogenesis.\n          <\/jats:p>","DOI":"10.1128\/jb.02284-14","type":"journal-article","created":{"date-parts":[[2014,12,23]],"date-time":"2014-12-23T06:17:36Z","timestamp":1419315456000},"page":"932-942","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":26,"title":["A\n            <i>prl<\/i>\n            Mutation in SecY Suppresses Secretion and Virulence Defects of Listeria monocytogenes secA2 Mutants"],"prefix":"10.1128","volume":"197","author":[{"given":"Juliana","family":"Durack","sequence":"first","affiliation":[{"name":"Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas P.","family":"Burke","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel A.","family":"Portnoy","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, California, USA"},{"name":"School of Public Health, University of California Berkeley, Berkeley, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamem.2010.08.016"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1098\/rstb.2011.0201"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.resmic.2013.03.007"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-011-0681-y"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7600804"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.tim.2007.03.001"},{"key":"e_1_3_3_8_2","doi-asserted-by":"crossref","first-page":"3391","DOI":"10.1002\/j.1460-2075.1993.tb06013.x","article-title":"PrlA suppressor mutations cluster in regions corresponding to three distinct topological domains","volume":"12","author":"Osborne RS","year":"1993","unstructured":"Osborne RS, Silhavy TJ. 1993. 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