title: Saccharomyces cerevisiae GATA sequences function as TATA elements during nitrogen catabolite repression and when Gln3p is excluded from the nucleus by overproduction of Ure2p.
abstract: Saccharomyces cerevisiae selectively uses good nitrogen sources (glutamine) in preference to poor ones (proline) by repressing GATA factor-dependent transcription of the genes needed to transport and catabolize poor nitrogen sources, a physiological process designated nitrogen catabolite repression (NCR). We show that some NCR-sensitive genes (CAN1, DAL5, DUR1,2, and DUR3) produce two transcripts of slightly different sizes. Synthesis of the shorter transcript is NCR-sensitive and that of the longer transcript is not. The longer transcript also predominates in gln3Delta mutants irrespective of the nitrogen source provided. We demonstrate that the longer mRNA species arises through the use of an alternative transcription start site generated by Gln3p-binding sites (GATAAs) being able to act as surrogate TATA elements. The ability of GATAAs to serve as surrogate TATAs, i.e. when synthesis of the shorter, NCR-sensitive transcripts are inhibited, correlates with sequestration of enhanced green fluorescent protein (EGFP)-Gln3p in the cytoplasm in a way that is indistinguishable from that seen with EGFP-Ure2p. However, when the shorter, NCR-sensitive DAL5 transcript predominates, EGFP-Gln3p is nuclear. These data suggest that the mechanism underlying NCR involves the cytoplasmic association of Ure2p with Gln3p, an interaction that prevents Gln3p from reaching it is binding sites upstream of NCR-sensitive genes.
authors.affiliation: Department of Microbiology and Immunology, University of Tennessee, Memphis, Tennessee 38163, USA.
authors.forename: K H
authors.initials: KH
authors.lastname: Cox
authors.forename: R
authors.initials: R
authors.lastname: Rai
authors.forename: M
authors.initials: M
authors.lastname: Distler
authors.forename: J R
authors.initials: JR
authors.lastname: Daugherty
authors.forename: J A
authors.initials: JA
authors.lastname: Coffman
authors.forename: T G
authors.initials: TG
authors.lastname: Cooper
mesh_terms: D026905:Amino Acid Transport Systems; D001483:Base Sequence; D001665:Binding Sites; D002467:Cell Nucleus / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism*; D015966:Gene Expression Regulation, Fungal; D005979:Glutathione Peroxidase; D026901:Membrane Transport Proteins / Q000235:genetics*; D008969:Molecular Sequence Data; D009584:Nitrogen / Q000378:metabolism*; D011328:Prions; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000235:genetics; D012097:Repressor Proteins / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism*; D029701:Saccharomyces cerevisiae Proteins; D014157:Transcription Factors; D014158:Transcription, Genetic
chemical_list: D026905:Amino Acid Transport Systems; C097640:CAN1 protein, Candida albicans; D004268:DNA-Binding Proteins; D005656:Fungal Proteins; C071664:GLN3 protein, S cerevisiae; D026901:Membrane Transport Proteins; D011328:Prions; D012333:RNA, Messenger; D012097:Repressor Proteins; D029701:Saccharomyces cerevisiae Proteins; D014157:Transcription Factors; D005979:Glutathione Peroxidase; C067020:URE2 protein, S cerevisiae; D009584:Nitrogen