Journal
EUKARYOTIC CELL
Volume 3, Issue 1, Pages 108-120Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/EC.3.1.108-120.2004
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Funding
- NCI NIH HHS [CA41086, P01 CA041086] Funding Source: Medline
- NIGMS NIH HHS [F32 GM019308, 5F32 GM19308] Funding Source: Medline
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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 G, delay that is accompanied by an increase in size, suggesting a G(1)/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.
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