Title: | Genetic evidence for the roles of the bud-site-selection genes BUD5 and BUD2 in control of the Rsr1p (Bud1p) GTPase in yeast |
Address: | "Department of Biology, Indiana University, Bloomington 47405" |
ISSN/ISBN: | 0027-8424 (Print) 1091-6490 (Electronic) 0027-8424 (Linking) |
Abstract: | "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" |
Keywords: | "*Cell Cycle Proteins GTP Phosphohydrolases/*biosynthesis/genetics *Genes, Fungal *Guanine Nucleotide Exchange Factors Mating Factor Peptides/genetics Pheromones/genetics Proto-Oncogene Proteins/biosynthesis/genetics Saccharomyces cerevisiae/*genetics/grow;" |
Notes: | "MedlineBender, A eng RR7031-26/RR/NCRR NIH HHS/ Research Support, U.S. Gov't, P.H.S. 1993/11/01 Proc Natl Acad Sci U S A. 1993 Nov 1; 90(21):9926-9. doi: 10.1073/pnas.90.21.9926" |