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Inhibition of Gl cyclin activity by the Ras/cAMP pathway in yeast

Abstract

IN the yeast Saccharomyces cerevisiae, commitment to cell division (Start) requires growth to a critical cell size1–3. The Gl cyclins Clnl, Cln2 and Cln3 activate the Cdc28 protein kinase and are rate-limiting activators of Start4–6. When glucose is added to cells growing in a poor carbon source, the critical cell size required for Start is reset from a small to a large size2,3,7. In yeast, glucose acts through Ras proteins to stimulate adenylyl cyclase, activating the three cyclic AMP-dependent protein kinases Tpkl, Tpk2 and Tpk3 (refs 8, 9). We find that stimulation of the Ras/cAMP pathway represses expression of CLN1, CLN2 and co-regulated genes, inhibiting Start. This helps explain the increase in critical size when cells are shifted from poor to rich medium. This connection between the molecules controlling growth (Ras/cAMP) and those controlling division (cyclins) helps explain how division is co-ordinated with growth.

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Tokiwa, G., Tyers, M., Volpe, T. et al. Inhibition of Gl cyclin activity by the Ras/cAMP pathway in yeast. Nature 371, 342–345 (1994). https://doi.org/10.1038/371342a0

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