ABSTRACT 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 ras2 Δ background. The slow-growth phenotype of mob2 Δ ras2 Δ cells results from a G 1 delay that is accompanied by an increase in size, suggesting a G 1 /S role for Ras not previously described. In addition, mob2 Δ 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.