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To investigate the specific target of PKA in the regulation of cell cycle progression and cell size we developed a new approach using the yeast strain GG104 bearing a deletion in adenylate cyclase gene and permeable to cAMP ( cyr1Δ, pde2Δ, msn2Δ, msn4Δ). In this strain the PKA activity is absent and can be activated by addition of cAMP in the medium, without any other change of the growth conditions. In the present work we show that the activation of PKA by exogenous cAMP in the GG104 strain exponentially growing in glucose medium caused a marked increase of cell size and perturbation of cell cycle with a transient arrest of cells in G1, followed by an accumulation of cells in G2/M phase with a minimal change in the growth rate. Deletion of CLN1gene, but not of CLN2, abolished the transient G1phase arrest. Consistently we found that PKA activation caused a transcriptional repression of CLN1gene. Transcription of CLN1is controlled by SBF and MBF dual-regulated promoter. We found that also the deletion of SWI4gene abolished the transient G1arrest suggesting that Swi4 is a target responsible for PKA modulation of G1/S phase transition. We generated a SWI4allele mutated in the consensus site for PKA (Swi4S159A) and we found that expression of Swi4S159Aprotein in the GG104-Swi4Δ strain did not restore the transient G1arrest induced by PKA activation, suggesting that Swi4 phosphorylation by PKA regulates CLN1gene expression and G1/S phase transition.