{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T02:52:45Z","timestamp":1790304765229,"version":"4.1.0"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"22","license":[{"start":{"date-parts":[[2015,11,15]],"date-time":"2015-11-15T00:00:00Z","timestamp":1447545600000},"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":["Appl Environ Microbiol"],"published-print":{"date-parts":[[2015,11,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            We previously demonstrated the clonal complex 81 (CC81) subtype 1 lineage is the major staphylococcal food poisoning (SFP)-associated lineage in Japan (Y. Sato'o et al., J Clin Microbiol\n            <jats:bold>52:<\/jats:bold>\n            2637\u20132640, 2014,\n            <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"http:\/\/dx.doi.org\/10.1128\/JCM.00661-14\">http:\/\/dx.doi.org\/10.1128\/JCM.00661-14<\/jats:ext-link>\n            ). Strains of this lineage produce staphylococcal enterotoxin H (SEH) in addition to SEA. However, an evaluation of the risk for the recently reported SEH has not been sufficiently conducted. We first searched for staphylococcal enterotoxin (SE) genes and SE proteins in milk samples that caused a large SFP outbreak in Japan. Only SEA and SEH were detected, while there were several SE genes detected in the samples. We next designed an experimental model using a meat product to assess the productivity of SEs and found that only SEA and SEH were detectably produced\n            <jats:italic>in situ<\/jats:italic>\n            . Therefore, we investigated the regulation of SEH production using a CC81 subtype 1 isolate. Through mutant analysis of global regulators, we found the repressor of toxin (Rot) functioned oppositely as a stimulator of SEH production. SEA production was not affected by Rot.\n            <jats:italic>seh<\/jats:italic>\n            mRNA expression correlated with\n            <jats:italic>rot<\/jats:italic>\n            both in media and on the meat product, and the Rot protein was shown to directly bind to the\n            <jats:italic>seh<\/jats:italic>\n            promoter. The\n            <jats:italic>seh<\/jats:italic>\n            promoter sequence was predicted to form a loop structure and to hide the RNA polymerase binding sequences. We propose Rot binds to the promoter sequence of\n            <jats:italic>seh<\/jats:italic>\n            and unfolds the secondary structure that may lead the RNA polymerase to bind the promoter, and then\n            <jats:italic>seh<\/jats:italic>\n            mRNA transcription begins. This alternative Rot regulation for SEH may contribute to sufficient toxin production by the CC81 subtype 1 lineage in foods to induce SFP.\n          <\/jats:p>","DOI":"10.1128\/aem.01936-15","type":"journal-article","created":{"date-parts":[[2015,9,5]],"date-time":"2015-09-05T02:39:35Z","timestamp":1441420775000},"page":"7782-7790","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":26,"title":["Positive Regulation of Staphylococcal Enterotoxin H by Rot (Repressor of Toxin) Protein and Its Importance in Clonal Complex 81 Subtype 1 Lineage-Related Food Poisoning"],"prefix":"10.1128","volume":"81","author":[{"given":"Yusuke","family":"Sato'o","sequence":"first","affiliation":[{"name":"Department of Bacteriology, Hiroshima University Graduate School of Biomedical &amp; Health Sciences, Hiroshima City, Hiroshima, Japan"},{"name":"The United Graduate School of Veterinary Sciences, Gifu University, Gifu City, Gifu, 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