title: The AFT1 transcriptional factor is differentially required for expression of high-affinity iron uptake genes in Saccharomyces cerevisiae.
abstract: High-affinity iron uptake in Saccharomyces cerevisiae involves the extracytoplasmic reduction of ferric ions by FRE1 and FRE2 reductases. Ferrous ions are then transported across the plasma membrane through the FET3 oxidase-FTR1 permease complex. Expression of the high-affinity iron uptake genes is induced upon iron deprivation. We demonstrate that AFT1 is differentially involved in such regulation. Aft1 protein is required for maintaining detectable non-induced level of FET3 expression and for induction of FRE2 in iron starvation conditions. On the contrary, FRE1 mRNA induction is normal in the absence of Aft1, although the existence of AFT1 point mutations causing constitutive expression of FRE1 (Yamaguchi-Iwai et al., EMBO J. 14: 1231-1239, 1995) indicates that Aft1 may also participate in FRE1 expression in a dispensable way. The alterations in the basal levels of expression of the high-affinity iron uptake genes may explain why the AFT1 mutant is unable to grow on respirable carbon sources. Overexpression of AFT1 leads to growth arrest of the G1 stage of the cell cycle. Aft1 is a transcriptional activator that would be part of the different transcriptional complexes interacting with the promoter of the high-affinity iron uptake genes. Aft1 displays phosphorylation modifications depending on the growth stage of the cells, and it might link induction of genes for iron uptake to other metabolically dominant requirement for cell growth.
authors.affiliation: Departament de Ciències Mèdiques Bàsiques, Facultat de Medicina, Universitat de Lleida, Spain.
authors.forename: C
authors.initials: C
authors.lastname: Casas
authors.forename: M
authors.initials: M
authors.lastname: Aldea
authors.forename: C
authors.initials: C
authors.lastname: Espinet
authors.forename: C
authors.initials: C
authors.lastname: Gallego
authors.forename: R
authors.initials: R
authors.lastname: Gil
authors.forename: E
authors.initials: E
authors.lastname: Herrero
mesh_terms: D002570:Ceruloplasmin; D003001:Cloning, Molecular; D000431:Ethanol / Q000378:metabolism; D038181:FMN Reductase; D005656:Fungal Proteins / Q000235:genetics* / Q000502:physiology*; D016193:G1 Phase; D015966:Gene Expression Regulation, Fungal; D005947:Glucose / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D007501:Iron / Q000378:metabolism*; D009247:NADH, NADPH Oxidoreductases / Q000235:genetics / Q000378:metabolism; D010088:Oxidoreductases / Q000235:genetics / Q000378:metabolism*; D010957:Plasmids; D017354:Point Mutation; D011401:Promoter Regions, Genetic; D012331:RNA, Fungal / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000235:genetics* / Q000254:growth & development; D029701:Saccharomyces cerevisiae Proteins; D017384:Sequence Deletion; D014157:Transcription Factors / Q000235:genetics* / Q000502:physiology*; D001616:beta-Galactosidase / Q000378:metabolism
chemical_list: C090297:AFT1 protein, S cerevisiae; D005656:Fungal Proteins; D012331:RNA, Fungal; D012333:RNA, Messenger; D029701:Saccharomyces cerevisiae Proteins; D014157:Transcription Factors; D000431:Ethanol; D007501:Iron; D010088:Oxidoreductases; D002570:Ceruloplasmin; C085513:FET3 protein, S cerevisiae; D038181:FMN Reductase; D009247:NADH, NADPH Oxidoreductases; C023903:ferric citrate iron reductase; D001616:beta-Galactosidase; D005947:Glucose; D005990:Glycerol