A pathogen such as C. albicans needs an efficient mechanism of iron uptake in an 
iron-restricted environment such as is the human body. A ferric-reductase 
activity regulated by iron and copper, and analogous to that in S. cerevisiae, 
has been described in C. albicans. We have developed an in-plate protocol for 
the isolation of clones that complement an aft1 mutation in S. cerevisiae that 
makes cells dependent on iron for growth. After transformation of S. cerevisiae 
aft1 with a C. albicans library, we have selected clones that grow in conditions 
of iron deficiency and share an identical plasmid, pIRO1, with a 4500 bp insert 
containing the URA3 gene and an ORF (IRO1) responsible for the suppression of 
the iron dependency. IRO1 does not show homology with AFT1 or with other 
sequences in the databases. Northern analysis demonstrates constitutive 
expression of IRO1. CAI4, a C. albicans strain isolated as Deltaura3, also has a 
deletion of the 3' half of IRO1, and displays in YNB medium similar phenotypic 
characteristics to S. cerevisiae aft1 mutant strains. Therefore, we consider 
IRO1 as a gene of C. albicans involved in the utilization of iron. However, in 
extreme conditions of iron deprivation, CAI4 seems to activate alternative 
mechanisms of iron uptake that allow a better growth than the wild strain 
SC5314. Analysis of its predicted protein sequence is in agreement with a role 
of Iro1p as a transcription factor.