Abstract
Abstract—Riboflavin (vitamin B2) is an important component of the diet of living organisms since it is a precursor of flavin coenzymes FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide) involved in numerous enzymatic reactions. It is known that flavinogenic yeast C. famata is able to perform riboflavin overproduction under conditions of iron deficiency, but the regulation of this process remains unknown. It was shown that the deletion of the SEF1 gene (encoding transcription activator) blocked the ability for riboflavin overproduction under conditions of iron deficiency. It was determined that SEF1 promoters of other flavinogenic yeasts (Candida albicans and Candida tropicalis) fused with SEF1 ORF of C. famata can restore the overproduction of riboflavin in the sef1Δ mutant. The disruption of the VMA1 gene (encoding the vacuolar ATPase subunit A) led to overproduction of riboflavin in C. famata in iron complete medium.
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