Entry into the cell cycle occurs only when sufficient growth has occurred. In budding yeast, the cyclin Cln3 is thought to initiate cell cycle entry by inactivating a transcriptional repressor called Whi5. Growth-dependent changes in the concentrations of Cln3 or Whi5 have been proposed to link cell cycle entry to cell growth. However, there are conflicting reports regarding the behavior and roles of Cln3 and Whi5. Here, we found no evidence that changes in the concentration of Whi5 play a major role in controlling cell cycle entry. Rather, the data suggest that cell growth triggers cell cycle entry by driving an increase in the concentration of Cln3. We further found that accumulation of Cln3 is dependent upon homologs of mammalian SGK kinases that control cell growth and size. Together, the data are consistent with models in which Cln3 is a crucial link between cell growth and the cell cycle.

Entry into the cell cycle occurs only when sufficient growth has occurred. In budding yeast, the cyclin Cln3 initiates cell cycle entry in late G1 phase by inactivating Whi5, a repressor that blocks transcription of genes that drive cell cycle entry. Growth-dependent changes in the concentrations of Cln3 and/or Whi5 have been proposed to link cell cycle entry to cell growth. However, there are conflicting reports regarding the behavior and roles of Cln3 and Whi5 during G1 phase, and little is known about the molecular mechanisms that link changes in their concentrations to cell growth. Here, we analyzed levels of Cln3 and Whi5 as a function of growth in G1 phase. We found no evidence that changes in the concentration of Whi5 play a major role in controlling cell cycle entry. Rather, the data are consistent with models in which a growth-dependent increase in the concentration of Cln3 drives cell cycle entry. We further found that Cln3 levels in G1 phase are strongly modulated by nutrient availability and by homologs of mammalian SGK kinases that are required for normal control of cell growth and size.

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