Abstract—Two Meyerozyma (Candida, Pichia) guilliermondii genes coding for homologs of transcriptional factor Sef1p of Candida famata and Tup1p of Candida albicans were identified, cloned, and deleted. Deletion of a homologue of Sef1p transcriptional factor in M.(P.) guilliermondii completely blocked over-synthesis of riboflavin under conditions of iron deficiency. The results of genetic complementation analysis suggest that previously reported rib83 mutants and newly constructed knock-out strains belong to the same complementation group and are defective in the same SEF1 gene. Inactivation of the identified homolog of the TUP1 gene in M.(P.) guilliermondii wild-type strain led to 1.5-fold increase in cellular iron content and 1.5–1.7-fold increase in riboflavin production. Introduction of a plasmid-borne copy of the TUP1 gene did not restore metabolic defects of the riboflavin overproduction and iron accumulation in mutant strain M. (P.) guilliermondii m3, bearing the hit1 mutation. The obtained results suggest that both transcription factors Sef1p and Tup1p are involved in the regulation of iron acquisition and riboflavin biosynthesis by yeast belonging to the CUG-clade. The molecular mechanism of action Tup1p on riboflavin biosynthesis in M.(P.) guilliermondii required further elucidation.

摘要—鉴定，克隆并删除了两个编码念珠菌的念珠菌（Pichia）和假丝酵母（Michierozyma）的假丝酵母基因，该基因分别编码念珠菌和白色念珠菌的转录因子Sef1p和Tup1p 。在缺铁条件下，在瓜德勒霉（M.（P.））中Sef1p转录因子的同源性的删除完全阻止了核黄素的过度合成。遗传互补分析的结果表明，先前报道的rib83突变体和新构建的敲除菌株属于同一互补组，并且在同一缺陷中SEF1基因。所述的鉴别的同源物的失活型TUP1基因在M.（P.）季也蒙野生型菌株导致细胞的铁含量增加1.5倍和在核黄素生产1.5-1.7倍的增加。TUP1基因的质粒携带的副本的引入不能恢复突变菌株M.（P.）guilliermondii中核黄素过量生产和铁积累的代谢缺陷m3，带有hit1突变。所得结果表明，转录因子Sef1p和Tup1p均参与了CUG-clade酵母对铁的获取和核黄素生物合成的调控。核黄素的生物合成在动作Tup1p的分子机制M.（P.）季也蒙需要进一步阐明。