Involvement of the Saccharomyces cerevisiae UTH1 gene in the oxidative-stress response

• Published in: Current genetics Vol. 34; no. 4; pp. 259 - 268
• Main Authors: Bandara, P.D.S, Flattery-O'Brien, J.A, Grant, C.M, Dawes, I.W
• Format: Journal Article
• Language: English
• Published: United States 01.10.1998
• Subjects: Amino Acid Sequence; amino acid sequences; beta-galactosidase; Cell Survival - genetics; Cloning, Molecular; deletions; Diamide - pharmacology; free radicals; Fungal Proteins - genetics; Gene Deletion; gene expression; Gene Expression Regulation, Fungal - drug effects; Genes, Fungal - genetics; genetic regulation; Heat-Shock Proteins - genetics; hydrogen peroxide; Hydrogen Peroxide - pharmacology; Membrane Proteins; Mitochondrial Proteins; Molecular Sequence Data; mortality; mutants; nucleotide sequences; nutrient deficiencies; oxidants; oxidation; Oxidative Stress - genetics; oxygen; paraquat; Paraquat - pharmacology; phenotype; promoter regions; proteins; recombinant DNA; reporter genes; Saccharomyces cerevisiae; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae Proteins; Sequence Analysis, DNA; Sequence Homology, Amino Acid; stress; structural genes; superoxide anion; Superoxides - pharmacology; transcription (genetics)
• ISSN: 0172-8083; 1432-0983
• DOI: 10.1007/s002940050395

The UTH1 gene was identified by screening a Saccharomyces cerevisiae promoter-probe gene bank for oxidative stress-responsive genes. Transcription of UTH1 was decreased by the superoxide anion and increased by hydrogen peroxide. Deletion of UTH1 did not affect the growth of grande cells, however in a rho0 background it caused retarded growth. The uth1 mutant showed increased resistance to peroxides and, in contrast, was sensitive to superoxide or the thiol oxidant diamide. Furthermore, the mutant exhibited increased survival under starvation conditions, with elevated levels of dormant cells in starved cell cultures. A multicopy plasmid containing the first half of the ORF could confer increased resistance to superoxide and increased sensitivity to peroxides/diamide/starvation on wild-type cells. The same plasmid in the uth1 background caused a highly increased mortality.