In Candida albicans, ergosterol biosynthetic genes, including ERG11 that encodes the target of azole antifungal drugs, are regulated by the transcriptional regulator Upc2p. To initially characterize the promoter of the UPC2 gene, 5' RACE was used to identify two transcriptional initiation sites upstream of the ATG. The regions within the UPC2 promoter required for azole regulation of the UPC2 promoter were then identified using nested deletions fused to a luciferase reporter which were tested for azole inducibility in wild type (WT) and upc2Delta/upc2Delta strains. Two distinct regions important for azole induction were identified: a Upc2p-dependent region (UDR) between -450 and -350 bp upstream of the ATG, and a Upc2p-independent region (UIR) between -350 and -250 bp upstream of the ATG. Within the Upc2p dependent UDR, loss or mutation of the SRE (sterol response element), so named because of homology to the S. cerevisiae Upc2p binding site, resulted in a decrease in both basal and induced expression in the WT strain, but did not affect azole inducibility in the upc2Delta/upc2Delta deletion strain. Gel shift analyses using the DNA binding domain of Upc2p confirmed binding of the protein to two SRE-related sequences within the UPC2 promoter, with strongest binding to the UDR SRE. Detailed gel shift analyses of the UDR SRE region shows that the Upc2p protein binds to a bipartite element within the UPC2 promoter, including the previously-identified SRE and a new, adjacent element, the short direct repeat (SDR), with partial homology to the SRE.