The dosage of the transcriptional activator ADR1 was varied in order to study the regulation of the glucose-repressible alcohol dehydrogenase (ADH II) from Saccharomyces cerevisiae. ADH II activity during glucose growth conditions was shown to increase linearly with increasing ADR1 gene dosage. In contrast, under derepressed growth conditions a 100-fold increase in ADR1 copy number resulted in only a 4-fold increase in ADH II expression. Saturation of ADH II gene expression by ADR1 under derepressed conditions was shown not to result from decreased ADR1 transcription. Increases in ADH2 gene dosage in conjunction with high ADR1 gene dosages resulted in increased ADH II activity, indicating that ADH2 was the limiting factor during derepression. Under glucose-repressed conditions the activator CCR1 was not required for ADR1 activity. During derepression increasing ADR1 dosage could partially compensate for a CCR1 defect. Increasing CCR1 gene dosage, however, had no effect on ADH2 expression regardless of the ADR1 allele present. These results suggest that CCR1 acts through ADR1 in controlling ADH2 expression. It was also observed that high numbers of ADR1, or a few copies of ADR1-5c, substantially increased the cell doubling time under ethanol growth conditions, indicating that increased ADR1 activity is toxic.