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.

中文翻译：

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调节基因 SEF1、VMA1 和 SFU1 在产黄素酵母念珠菌（Candidaflareri）核黄素合成中的作用。

核黄素或维生素 B ₂是人类和动物必不可少的膳食成分，它是参与众多酶促反应的黄素辅酶黄素单核苷酸和黄素腺嘌呤二核苷酸的前体。黄素酵母念珠菌在缺铁条件下过量产生核黄素；然而，对该过程的监管知之甚少。已经鉴定了编码转录激活因子的调节基因SEF1。它的缺失阻止了酵母在铁饥饿下过度产生核黄素的能力。这里显示，来自其他黄素（白色念珠菌）和非黄素（热带念珠菌）的SEF1启动子) 与来自C. famata的SEF1基因的开放阅读框 (ORF) 融合的酵母能够恢复sef1Δ突变体中核黄素的过度合成。已知在致病性黄素酵母C. albicans 中，Sfu1（GATA 型转录因子）抑制SEF1。在这里，我们发现野生型C. famata中SFU1基因的缺失导致核黄素过度合成。此外，已表明VMA1基因（编码液泡 ATP 酶亚基 A）的破坏也会导致C. famata中核黄素的过度合成。