CTR2 encodes a low-affinity copper transporter that mediates the mobilization of 
vacuolar copper stores in yeast. We previously reported that CTR2 can be 
upregulated by copper deficiency via copper-sensing transcription factor Mac1p. 
In the present study, we found that iron depletion also induces the 
transcription of CTR2. The upregulation of CTR2 induced by iron depletion was 
abrogated by the genetic deletion of either Mac1p or iron-sensing transcription 
factor Aft1p. The ablation of either MAC1 or AFT1 also abrogated CTR2 expression 
induced by copper depletion. Our further study revealed that exogenous Aft1p 
upregulates CTR2 transcription only in the presence of Mac1p, whereas exogenous 
Mac1p upregulates CTR2 transcription only in the presence of Aft1p. Exogenous 
Mac1p and Aft1p form a stable complex and synergistically enhance CTR2 
transcription. These data suggest that Aft1p and Mac1p might corporately 
regulate transcription of CTR2.