
The Ras/Protein Kinase A Pathway Acts in Parallel with the Mob2/Cbk1 Pathway To Effect Cell Cycle Progression and Proper Bud Site Selection
Author(s) -
Lisa Schneper,
Alicia Krauss,
Ryo Miyamoto,
Shirley Fang,
James R. Broach
Publication year - 2004
Publication title -
eukaryotic cell
Language(s) - English
Resource type - Journals
eISSN - 1535-9778
pISSN - 1535-9786
DOI - 10.1128/ec.3.1.108-120.2004
Subject(s) - biology , microbiology and biotechnology , transcription factor , phenotype , protein kinase a , saccharomyces cerevisiae , cell cycle , cell division , cell growth , mitosis , gene , protein subunit , cell , kinase , genetics
In Saccharomyces cerevisiae, Ras proteins connect nutrient availability to cell growth through regulation of protein kinase A (PKA) activity. Ras proteins also have PKA-independent functions in mitosis and actin repolarization. We have found that mutations in MOB2 or CBK1 confer a slow-growth phenotype in a ras2Delta background. The slow-growth phenotype of mob2Delta ras2Delta cells results from a G1 delay that is accompanied by an increase in size, suggesting a G1/S role for Ras not previously described. In addition, mob2Delta strains have imprecise bud site selection, a defect exacerbated by deletion of RAS2. Mob2 and Cbk1 act to properly localize Ace2, a transcription factor that directs daughter cell-specific transcription of several genes. The growth and budding phenotypes of the double-deletion strains are Ace2 independent but are suppressed by overexpression of the PKA catalytic subunit, Tpk1. From these observations, we conclude that the PKA pathway and Mob2/Cbk1 act in parallel to determine bud site selection and promote cell cycle progression.