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.

摘要—核黄素（维生素B ₂）是活生物体饮食的重要组成部分，因为它是黄素辅酶FMN（黄素单核苷酸）和FAD（黄素腺嘌呤二核苷酸）的前体，参与许多酶促反应。众所周知，在铁缺乏的条件下，产黄酵母的C. famata酵母能够执行核黄素的过量生产，但是该过程的调控仍然未知。结果表明，在缺铁条件下，SEF1基因的缺失（编码转录激活因子）阻止了核黄素的过度生产。经测定，SEF1其他flavinogenic酵母的启动子（白色念珠菌和热带假丝酵母）具有稠合SEF1的ORF C. famata可以在恢复核黄素的生产过剩sef1Δ突变体。VMA1基因（编码液泡ATPase亚基A）的破坏导致铁完全培养基中法氏梭菌核黄素的过量生产。