title: Iron uptake by the yeast Pichia guilliermondii. Flavinogenesis and reductive iron assimilation are co-regulated processes.
abstract: Pichia guilliermondii cells overproduce riboflavin (vitamin B2) in responce to iron deprivation. The increase in ferrireductase activity in iron-starved P. guilliermondii cells correlated with the increase in flavin excretion. As in Saccharomyces cerevisiae, a typical b-type cytochrome spectrum was associated with the plasma membrane fraction of P. guilliermondii and the cell ferrireductase activity was strongly inhibited by diphenylene-iodonium, an inhibitor of flavoproteins, in both yeasts. Mutants of P. guilliermondii with increased ferrireductase activity were selected for further investigation of the relationship between iron reduction/uptake and flavin production. The obtained mutation has been called hit (high iron transport). A hit mutant with a single recessive mutation showed the following phenotype: high ferrireductase activity, increased rate of iron uptake and elevated flavinogenic activity. Cu(II) (50 microns) strongly inhibited the growth of the hit mutant compared to the wild-type. The mutant cells grown in copper-supplemented medium (5-25 microns) showed an increase of the ferrireductase activity (up to 2-3 fold). The copper content of the mutant cells grown under these conditions was also higher (1.5-2 fold) than that of the wild-type. The role of the HIT gene of P. guillermondii in the regulation of iron, copper and flavin metabolisms is discussed.
authors.affiliation: Division of Regulatory Cell Systems, A. V. Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Lviv.
authors.forename: D
authors.initials: D
authors.lastname: Fedorovich
authors.forename: O
authors.initials: O
authors.lastname: Protchenko
authors.forename: E
authors.initials: E
authors.lastname: Lesuisse
mesh_terms: D001692:Biological Transport; D002462:Cell Membrane / Q000201:enzymology; D003300:Copper / Q000494:pharmacology; D003573:Cytochrome b Group / Q000378:metabolism; D038181:FMN Reductase; D005415:Flavins / Q000378:metabolism*; D005838:Genotype; D007501:Iron / Q000378:metabolism*; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D010084:Oxidation-Reduction; D010843:Pichia / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D012256:Riboflavin / Q000096:biosynthesis
chemical_list: D003573:Cytochrome b Group; D005415:Flavins; D003300:Copper; D007501:Iron; D038181:FMN Reductase; D009247:NADH, NADPH Oxidoreductases; C023903:ferric citrate iron reductase; D012256:Riboflavin