Genetic evidence for the roles of the bud-site-selection genes BUD5 and BUD2 in control of the Rsr1p (Bud1p) GTPase in yeast
| Autor: | Alan Bender |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Saccharomyces cerevisiae Proteins
Genes Fungal Mutant Saccharomyces cerevisiae Cell Cycle Proteins GTPase Pheromones GTP Phosphohydrolases law.invention Gene product Suppression Genetic law Proto-Oncogene Proteins Guanine Nucleotide Exchange Factors Ras2 Gene Genetics Multidisciplinary biology biology.organism_classification Phenotype rab GTP-Binding Proteins Suppressor Mating Factor Peptides Research Article |
| Zdroj: | Proceedings of the National Academy of Sciences. 90:9926-9929 |
| ISSN: | 1091-6490 0027-8424 |
| DOI: | 10.1073/pnas.90.21.9926 |
| Popis: | Yeast cells normally display either an axial (for MATa or MAT alpha cells) or bipolar (for MATa/alpha cells) pattern of bud-site selection. The RSR1 gene, which was previously identified as a multicopy suppressor of Ts- mutations in the bud-emergence gene CDC24, encodes a GTPase of the Ras family that is required for both budding patterns. Mutations in Rsr1p that presumably block its ability to bind or hydrolyze GTP cause a randomized budding phenotype, suggesting that regulators of Rsr1p will prove to be required for proper bud positioning. The BUD5 gene product is required for proper bud-site selection and contains similarity to GDP-dissociation stimulators (GDS) for Ras-type proteins, suggesting that Bud5p may be a GDS for Rsr1p. Here I report that BUD5 is required for wild-type RSR1, but not for mutationally activated rsr1val12, to serve as a multicopy suppressor of cdc24, indicating that Bud5p functions as a GDS for Rsr1p in vivo. To identify the GAP (GTPase-activating protein) for Rsr1p, a genetic selection was designed based on the observation that mutationally activated rsr1val12, but not wild-type RSR1, can serve as a multicopy suppressor of yeast RAS2(Ts) mutants. Mutants were selected that allowed wild-type RSR1 to act as a multicopy suppressor of RAS2(Ts). Two such mutations proved to be in the BUD2 gene, suggesting that Bud2p functions as a GAP for Rsr1p in vivo. |
| Databáze: | OpenAIRE |
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