{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T18:54:03Z","timestamp":1791140043897,"version":"4.1.0"},"reference-count":29,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2007,4,15]],"date-time":"2007-04-15T00:00:00Z","timestamp":1176595200000},"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":["J Bacteriol"],"published-print":{"date-parts":[[2007,4,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>MgrA is a known regulator of the expression of several multidrug transporters in<jats:italic>Staphylococcus aureus<\/jats:italic>. We identified another regulator of multiple efflux pumps, NorG, by its ability, like that of MgrA, to bind specifically to the promoter of the gene encoding the NorA efflux pump. NorG is a member of the family of the GntR-like transcriptional regulators, and it binds specifically to the putative promoters of the genes encoding multidrug efflux pumps NorA, NorB, NorC, and AbcA. Overexpression of<jats:italic>norG<\/jats:italic>produces a threefold increase in<jats:italic>norB<\/jats:italic>transcripts associated with a fourfold increase in the level of resistance to quinolones. In contrast, disruption of<jats:italic>norG<\/jats:italic>produces no change in the level of transcripts of<jats:italic>norA<\/jats:italic>,<jats:italic>norB<\/jats:italic>, and<jats:italic>norC<\/jats:italic>but causes an increase of at least threefold in the transcript level of<jats:italic>abcA<\/jats:italic>, associated with a fourfold increase in resistance to methicillin, cefotaxime, penicillin G, and nafcillin. Overexpression of cloned<jats:italic>abcA<\/jats:italic>caused an 8- to 128-fold increase in the level of resistance to all four \u03b2-lactam antibiotics. Furthermore, MgrA and NorG have opposite effects on<jats:italic>norB<\/jats:italic>and<jats:italic>abcA<\/jats:italic>expression. MgrA acts as an indirect repressor for<jats:italic>norB<\/jats:italic>and a direct activator for<jats:italic>abcA<\/jats:italic>, whereas NorG acts as a direct activator for<jats:italic>norB<\/jats:italic>and a direct repressor for<jats:italic>abcA<\/jats:italic>.<\/jats:p>","DOI":"10.1128\/jb.01819-06","type":"journal-article","created":{"date-parts":[[2007,2,4]],"date-time":"2007-02-04T01:19:29Z","timestamp":1170551969000},"page":"2996-3005","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":98,"title":["The Transcriptional Regulators NorG and MgrA Modulate Resistance to both Quinolones and \u03b2-Lactams in<i>Staphylococcus aureus<\/i>"],"prefix":"10.1128","volume":"189","author":[{"given":"Que Chi","family":"Truong-Bolduc","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases and Medical Services, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114-2696"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David C.","family":"Hooper","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases and Medical Services, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114-2696"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"245","DOI":"10.1093\/jac\/29.3.245","volume":"29","year":"1992","unstructured":"Chopra, I., P. 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