Catabolite inactivation of the galactose transporter in the yeast Saccharomyces cerevisiae: ubiquitination, endocytosis, and degradation in the vacuole
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
9045811
PubMed Central
PMC178864
DOI
10.1128/jb.179.5.1541-1549.1997
Knihovny.cz E-resources
- MeSH
- Sodium Azide MeSH
- Azides pharmacology MeSH
- Cycloheximide pharmacology MeSH
- Cytoplasm metabolism MeSH
- Cytoskeletal Proteins * MeSH
- Endocytosis * MeSH
- Fungal Proteins metabolism MeSH
- Galactose metabolism MeSH
- Glucose pharmacology MeSH
- Protein Synthesis Inhibitors pharmacology MeSH
- Monosaccharide Transport Proteins metabolism MeSH
- Saccharomyces cerevisiae Proteins * MeSH
- Saccharomyces cerevisiae metabolism MeSH
- Temperature MeSH
- Ubiquitins metabolism MeSH
- Vacuoles metabolism MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Sodium Azide MeSH
- Azides MeSH
- Cycloheximide MeSH
- Cytoskeletal Proteins * MeSH
- END3 protein, S cerevisiae MeSH Browser
- Fungal Proteins MeSH
- Galactose MeSH
- Glucose MeSH
- Protein Synthesis Inhibitors MeSH
- Monosaccharide Transport Proteins MeSH
- Saccharomyces cerevisiae Proteins * MeSH
- Ubiquitins MeSH
When Saccharomyces cerevisiae cells growing on galactose are transferred onto glucose medium containing cycloheximide, an inhibitor of protein synthesis, a rapid reduction of Gal2p-mediated galactose uptake is observed. We show that glucose-induced inactivation of Gal2p is due to its degradation. Stabilization of Gal2p in pra1 mutant cells devoid of vacuolar proteinase activity is observed. Subcellular fractionation and indirect immunofluorescence showed that the Gal2 transporter accumulates in the vacuole of the mutant cells, directly demonstrating that its degradation requires vacuolar proteolysis. In contrast, Gal2p degradation is proteasome independent since its half-life is unaffected in pre1-1 pre2-2, cim3-1, and cim5-1 mutants defective in several subunits of the protease complex. In addition, vacuolar delivery of Gal2p was shown to be blocked in conditional end3 and end4 mutants at the nonpermissive temperature, indicating that delivery of Gal2p to the vacuole occurs via the endocytic pathway. Taken together, the results presented here demonstrate that glucose-induced proteolysis of Gal2p is dependent on endocytosis and vacuolar proteolysis and is independent of the functional proteasome. Moreover, we show that Gal2p is ubiquitinated under conditions of glucose-induced inactivation.
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