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In the present study, we have examined the role of both SarA and RNAIII on the regulation of the promoter of\n            <jats:italic>tst<\/jats:italic>\n            , encoding staphylococcal superantigen toxic shock syndrome toxin 1 (TSST-1).\n            <jats:italic>In vitro<\/jats:italic>\n            DNA-protein interaction studies with purified SarA using gel shift and DNase I protection assays revealed one strong SarA binding site and evidence for a weaker site nearby within the minimal 400-bp promoter region upstream of\n            <jats:italic>tst. In vivo<\/jats:italic>\n            analysis of\n            <jats:italic>tst<\/jats:italic>\n            promoter activation using a\n            <jats:italic>\n              p\n              <jats:sub>tst<\/jats:sub>\n            <\/jats:italic>\n            -\n            <jats:italic>luxAB<\/jats:italic>\n            reporter inserted in the chromosome revealed partial but not complete loss of\n            <jats:italic>tst<\/jats:italic>\n            expression in a \u0394\n            <jats:italic>hld<\/jats:italic>\n            -\n            <jats:italic>RNAIII<\/jats:italic>\n            strain. In contrast, disruption of\n            <jats:italic>sarA<\/jats:italic>\n            abrogated\n            <jats:italic>tst<\/jats:italic>\n            expression. No significant\n            <jats:italic>tst<\/jats:italic>\n            expression was found for the double \u0394\n            <jats:italic>hld-RNAIII-<\/jats:italic>\n            \u0394\n            <jats:italic>sarA<\/jats:italic>\n            mutant. Introduction of a plasmid containing cloned\n            <jats:italic>hld-RNAIII<\/jats:italic>\n            driven by a non-\n            <jats:italic>agr<\/jats:italic>\n            -dependent promoter,\n            <jats:italic>\n              p\n              <jats:sub>HU<\/jats:sub>\n            <\/jats:italic>\n            , into isogenic parental wild-type or \u0394\n            <jats:italic>sarA<\/jats:italic>\n            strains showed comparable levels of RNAIII detected by quantitative reverse transcription-PCR (qRT-PCR) but a two-log\n            <jats:sub>10<\/jats:sub>\n            reduction in\n            <jats:italic>\n              p\n              <jats:sub>tst<\/jats:sub>\n              -luxAB\n            <\/jats:italic>\n            reporter expression in the \u0394\n            <jats:italic>sarA<\/jats:italic>\n            strain, arguing that RNAIII levels alone are not strictly determinant for\n            <jats:italic>tst<\/jats:italic>\n            expression. Collectively, our results indicate that SarA binds directly to the\n            <jats:italic>tst<\/jats:italic>\n            promoter and that SarA plays a significant and direct role in the expression of\n            <jats:italic>tst<\/jats:italic>\n            .\n          <\/jats:p>","DOI":"10.1128\/jb.00146-10","type":"journal-article","created":{"date-parts":[[2010,9,25]],"date-time":"2010-09-25T02:50:47Z","timestamp":1285383047000},"page":"6077-6085","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":45,"title":["Control of the\n            <i>Staphylococcus aureus<\/i>\n            Toxic Shock\n            <i>tst<\/i>\n            Promoter by the Global Regulator SarA"],"prefix":"10.1128","volume":"192","author":[{"given":"Diego O.","family":"Andrey","sequence":"first","affiliation":[{"name":"Service of Infectious Diseases, University Hospital and Medical School of Geneva, 4 rue Gabrielle-Perret-Gentil, CH-1211 Geneva 14, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adriana","family":"Renzoni","sequence":"additional","affiliation":[{"name":"Service of Infectious Diseases, University Hospital and Medical School of Geneva, 4 rue Gabrielle-Perret-Gentil, CH-1211 Geneva 14, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antoinette","family":"Monod","sequence":"additional","affiliation":[{"name":"Service of Infectious Diseases, University Hospital and Medical School of Geneva, 4 rue Gabrielle-Perret-Gentil, CH-1211 Geneva 14, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel P.","family":"Lew","sequence":"additional","affiliation":[{"name":"Service of Infectious Diseases, University Hospital and Medical School of Geneva, 4 rue Gabrielle-Perret-Gentil, CH-1211 Geneva 14, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ambrose L.","family":"Cheung","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Dartmouth Medical School, Hanover, New Hampshire"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William L.","family":"Kelley","sequence":"additional","affiliation":[{"name":"Service of Infectious Diseases, University Hospital and Medical School of Geneva, 4 rue Gabrielle-Perret-Gentil, CH-1211 Geneva 14, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.01202-09"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.183.17.5171-5179.2001"},{"key":"e_1_3_2_4_2","doi-asserted-by":"crossref","first-page":"317","DOI":"10.1046\/j.1365-2958.1999.01475.x","volume":"33","year":"1999","unstructured":"Blevins, J. 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