Investigation Title Transcription profiling of mutations in the yeast TRR1 gene encoding thioredoxin reductase Comment[Submitted Name] Carmel-Harel et al Experimental Design time_series_design transcription profiling by array Experimental Design Term Source REF mo EFO Comment[ArrayExpressReleaseDate] 2005-06-30 Comment[AEMIAMESCORE] 4 Comment[ArrayExpressAccession] E-SMDB-2716 Comment[MAGETAB TimeStamp_Version] 2011-01-23 13:59:46 Last Changed Rev: 14857 Experimental Factor Name Experimental Factor Type Experimental Factor Term Source REF Person Last Name Iyer Gasch Boussard Person First Name Vishy Audrey Tina Person Mid Initials Person Email vishy@icmb.utexas.edu apgasch@lbl.gov boussard@genome.stanford.edu Person Phone 650-723-6902 (650)725-6376 650-736-0077 Person Fax 650-725-7811 (650)725-6044 650-723-7016 Person Address School of Medicine, Department of Biochemistry, Stanford, CA, USA, 94305 Department of Biochemistry, Beckman Center B400, Stanford University School of Medicine, Stanford, CA, USA, 94305-5307 School of Medicine, Department of Genetics, Stanford, CA, United States, 94305 Person Affiliation Stanford University Stanford University Stanford University Person Roles submitter submitter submitter Person Roles Term Source REF mo mo mo Quality Control Type Quality Control Term Source REF Replicate Type Replicate Term Source REF Normalization Type Normalization Term Source REF Date of Experiment Public Release Date 2005-06-30 PubMed ID 11169101 Publication DOI 11169101 Publication Author List Carmel-Harel O, Stearman R, Gasch AP, Botstein D, Brown PO, Storz G Publication Title Role of thioredoxin reductase in the Yap1p-dependent response to oxidative stress in Saccharomyces cerevisiae. Publication Status journal_article Publication Status Term Source REF Experiment Description The Saccharomyces cerevisiae Yap1p transcription factor is required for the H2O2-dependent activation of many antioxidant genes including the TRX2 gene encoding thioredoxin 2. To identify factors that regulate Yap1p activity, we carried out a genetic screen for mutants that show elevated expression of a TRX2-HIS3 fusion in the absence of H2O2. Two independent mutants isolated in this screen carried mutations in the TRR1 gene encoding thioredoxin reductase. Northern blot and whole-genome expression analysis revealed that the basal expression of most Yap1p targets and many other H2O2-inducible genes is elevated in Deltatrr1 mutants in the absence of external stress. In Deltatrr1 mutants treated with H2O2, the Yap1p targets, as well as genes comprising a general environmental stress response and genes encoding protein-folding chaperones, are hyperinduced. However, despite the elevated expression of genes encoding antioxidant enzymes, Deltatrr1 mutants are extremely sensitive to H2O2. The results suggest that cells lacking thioredoxin reductase have diminished capacity to detoxify oxidants and/or to repair oxidative stress-induced damage and that the thioredoxin system is involved in the redox regulation of Yap1p transcriptional activity. Protocol Name Protocol Type Protocol Description Protocol Parameters Protocol Hardware Protocol Software Protocol Contact Protocol Term Source REF SDRF File E-SMDB-2716.sdrf.txt Term Source Name ncbitax mo ArrayExpress mo EFO Term Source File http://www.ncbi.nlm.nih.gov/Taxonomy/taxonomyhome.html http://mged.sourceforge.net/ontologies/MGEDontology.php http://www.ebi.ac.uk/arrayexpress http://mged.sourceforge.net/ontologies/MGEDontology.php http://www.ebi.ac.uk/efo/ Term Source Version