RESUMO
Riboflavin or vitamin B2 is an essential dietary component for humans and animals that is the precursor of flavin coenzymes flavin mononucleotide and flavin adenine dinucleotide involved in numerous enzymatic reactions. The flavinogenic yeast Candida famata overproduces riboflavin under iron starvation; however, regulation of this process is poorly understood. Regulatory gene SEF1 encoding transcription activator has been identified. Its deletion blocks yeast ability to overproduce riboflavin under iron starvation. It was shown here that the SEF1 promoters from other flavinogenic (Candida albicans) and non-flavinogenic (Candida tropicalis) yeasts fused with the open reading frame (ORF) of SEF1 gene from C. famata are able to restore riboflavin oversynthesis in sef1Δ mutants. It is known that in the pathogenic flavinogenic yeast C. albicans, Sfu1 (GATA-type transcription factor) represses SEF1. Here, we found that deletion of SFU1 gene in wild-type C. famata leads to riboflavin oversynthesis. Moreover, it was shown that disruption of VMA1 gene (coding for vacuolar ATPase subunit A) also results in riboflavin oversynthesis in C. famata.
