{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,30]],"date-time":"2026-08-30T12:43:15Z","timestamp":1788093795786,"version":"build-2803163510"},"reference-count":50,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,5,20]],"date-time":"2013-05-20T00:00:00Z","timestamp":1369008000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Yeast"],"published-print":{"date-parts":[[2013,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Pdr16p belongs to the family of phosphatidylinositol transfer proteins in yeast. The absence of Pdr16p results in enhanced susceptibility to azole antifungals in <jats:italic>Saccharomyces cerevisiae<\/jats:italic>. In the major fungal human pathogen <jats:italic>Candida albicans<\/jats:italic>, <jats:italic>CaPDR16<\/jats:italic> is a contributing factor to clinical azole resistance. The current study was aimed at better understanding the function of Pdr16p, especially in relation to azole resistance in <jats:italic>S<\/jats:italic>. <jats:italic>cerevisiae<\/jats:italic>. We show that deletion of the <jats:italic>PDR16<\/jats:italic> gene increased susceptibility of <jats:italic>S<\/jats:italic>. <jats:italic>cerevisiae<\/jats:italic> to azole antifungals that are used in clinical medicine and agriculture. Significant differences in the inhibition of the sterol biosynthetic pathway were observed between the <jats:italic>pdr16\u0394<\/jats:italic> strain and its corresponding wild\u2010type (wt) strain when yeast cells were challenged by sub\u2010inhibitory concentrations of the azoles miconazole or fluconazole. The increased susceptibility to azoles, and enhanced changes in sterol biosynthesis upon exposure to azoles of the <jats:italic>pdr16\u0394<\/jats:italic> strain compared to wt strain, are not the results of increased intracellular concentration of azoles in the <jats:italic>pdr16\u0394<\/jats:italic> cells. We also show that overexpression of <jats:italic>PDR17<\/jats:italic> complemented the azole susceptible phenotype of the <jats:italic>pdr16\u0394<\/jats:italic> strain and corrected the enhanced sterol alterations in <jats:italic>pdr16\u0394<\/jats:italic> cells in the presence of azoles. Pdr17p was found previously to be an essential part of a complex required for intermembrane transport of phosphatidylserine at regions of membrane apposition. Based on these observations, we propose a hypothesis that Pdr16p assists in shuttling sterols or their intermediates between membranes or, alternatively, between sterol biosynthetic enzymes or complexes. Copyright \u00a9 2013 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/yea.2956","type":"journal-article","created":{"date-parts":[[2013,4,19]],"date-time":"2013-04-19T09:46:51Z","timestamp":1366364811000},"page":"229-241","source":"Crossref","is-referenced-by-count":25,"title":["The yeast <i>Saccharomyces cerevisiae<\/i> Pdr16p restricts changes in ergosterol biosynthesis caused by the presence of azole antifungals"],"prefix":"10.1002","volume":"30","author":[{"given":"Zuzana","family":"\u0160imov\u00e1","sequence":"first","affiliation":[{"name":"Institute of Animal Biochemistry and Genetics Slovak Academy of Sciences  Ivanka pri Dunaji Slovakia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katar\u00edna","family":"Poloncov\u00e1","sequence":"additional","affiliation":[{"name":"Institute of Animal Biochemistry and Genetics Slovak Academy of Sciences  Ivanka pri Dunaji 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