Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1990 Jun;17(6):465-72.
doi: 10.1007/BF00313073.

Isolation and genetic study of triethyltin-resistant mutants of Saccharomyces cerevisiae

Affiliations

Isolation and genetic study of triethyltin-resistant mutants of Saccharomyces cerevisiae

C H Dupont et al. Curr Genet. 1990 Jun.

Abstract

Three mutants of Saccharomyces cerevisiae resistant to triethyltin (an inhibitor of mitochondrial ATPase) on non-fermentative media, and non-resistant to this drug on fermentative media, were isolated and named TTR1, TTR2 and TTR3. Apart from triethyltin resistance, these mutants show the following common characteristics: (1) Increased intracellular cytochrome c concentration. (2) Increased respiration rate. (3) Decreased growth yield. (4) Increased growth sensitivity to several drugs inhibiting oxidative phosphorylation: namely, CCCP (permeabilizing inner mitochondrial membrane to protons), valinomycin (permeabilizing inner mitochondrial membrane to potassium) and oligomycin (inhibitor of mitochondrial ATPase). (5) Increased sensitivity to carbon source starvation. For each mutant, these characteristics appeared to be due to a single pleiotropic nuclear mutation. Mutation TTR1 causes additional phenotypic characteristics which do not appear in mutants TTR2 and TTR3: (1) Pinkish coloration of colonies which is more pronounced after a long growth period. (2) Inability of the cells to store glycogen. (3) Growth defect of the cells on a galactose-containing medium. (4) Inability of a diploid homozygote mutant strain to sporulate. All these phenotypic characteristics have already been described in yeast mutants deregulated in cAMP-dependent protein phosphorylation. Crossing of a strain bearing the TTR1 mutation with a strain mutated in the adenylate cyclase structural gene suggested that the TTR1 phenotype is due to a modification in regulation of cAPK by cAMP, making cell multiplication possible without intracellular cAMP.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Eur J Biochem. 1975 Feb 21;51(2):377-92 - PubMed
    1. J Bacteriol. 1986 May;166(2):364-7 - PubMed
    1. Mol Gen Genet. 1974;134(3):261-72 - PubMed
    1. J Bacteriol. 1984 Jan;157(1):277-82 - PubMed
    1. Annu Rev Biochem. 1979;48:923-59 - PubMed

Publication types

LinkOut - more resources