{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T09:26:59Z","timestamp":1768469219598,"version":"3.49.0"},"reference-count":45,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2011,6,5]],"date-time":"2011-06-05T00:00:00Z","timestamp":1307232000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2011,7]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>ToxR of <jats:italic>Vibrio cholerae<\/jats:italic> directly activates the <jats:italic>ompU<\/jats:italic> promoter, but requires a second activator, TcpP to activate the <jats:italic>toxT<\/jats:italic> promoter. <jats:italic>ompU<\/jats:italic> encodes a porin, while <jats:italic>toxT<\/jats:italic> encodes the transcription factor, ToxT, which activates <jats:italic>V. cholerae<\/jats:italic> virulence genes including cholera toxin and the toxin co\u2010regulated pilus. Using an <jats:italic>ompU\u2010sacB<\/jats:italic> transcriptional fusion, <jats:italic>toxR<\/jats:italic> mutant alleles were identified that encode ToxR molecules defective for <jats:italic>ompU<\/jats:italic> promoter activation. Many <jats:italic>toxR<\/jats:italic> mutants defective for <jats:italic>ompU<\/jats:italic> activation affected residues involved in DNA binding. Mutants defective for <jats:italic>ompU<\/jats:italic> activation were also tested for activation of the <jats:italic>toxT<\/jats:italic> promoter. ToxR\u2010F69A and ToxR\u2010V71A, both in the \u03b1\u2010loop of ToxR, were preferentially defective for <jats:italic>ompU<\/jats:italic> activation, with ToxR\u2010V71A nearly completely defective. Six mutants from the <jats:italic>ompU\u2010sacB<\/jats:italic> selection showed more dramatic defects in <jats:italic>toxT<\/jats:italic> activation than <jats:italic>ompU<\/jats:italic> activation. All but one of the affected residues map to the wing domain of the winged helix\u2013turn\u2013helix of ToxR. Some ToxR mutants preferentially affecting <jats:italic>toxT<\/jats:italic> activation had partial DNA\u2010binding defects, and one mutant, ToxR\u2010P101L, had altered interactions with TcpP. These data suggest that while certain residues in the \u03b1\u2010loop of ToxR are utilized to activate the <jats:italic>ompU<\/jats:italic> promoter, the wing domain of ToxR contributes to both promoter binding and ToxR\/TcpP interaction facilitating <jats:italic>toxT<\/jats:italic> activation.<\/jats:p>","DOI":"10.1111\/j.1365-2958.2011.07681.x","type":"journal-article","created":{"date-parts":[[2011,5,4]],"date-time":"2011-05-04T10:14:34Z","timestamp":1304504074000},"page":"113-128","source":"Crossref","is-referenced-by-count":26,"title":["The two faces of ToxR: activator of <i>ompU<\/i>, co\u2010regulator of <i>toxT<\/i> in <i>Vibrio cholerae<\/i>"],"prefix":"10.1111","volume":"81","author":[{"given":"Sarah 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