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A likely contributor to the increased incidence of non- albicans  candidemias involving  Candida glabrata  is the ease with which this yeast acquires azole resistance, in large part due to induction of the ATP-binding cassette transporter-encoding gene  CDR1 . Azole drugs lead to induction of Pdr1 transactivation, with a central model being that this factor binds these drugs directly. Here we provide evidence that Pdr1 is activated without azole drugs by the use of genetic means to inhibit expression of azole drug target-encoding gene  ERG11 . These acute reductions in Erg11 levels lead to elevated Pdr1 activity even though no drug is present. A key transcriptional regulator of the  ERG  pathway, Upc2A, is shown to directly bind to the  PDR1  and  CDR1  promoters. We interpret these data as support for the view that Pdr1 function is responsive to ergosterol biosynthesis and suggest that this connection reveals the normal physiological circuitry in which Pdr1 participates.

Evidence that Ergosterol Biosynthesis Modulates Activity of the Pdr1 Transcription Factor in Candida glabrata