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

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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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Author notes

  1. George Tokiwa and Tom Volpe: Graduate Program in Genetics, State University of New York, Stony Brook, New York 11792, USA

  2. Mike Tyers: Banting and Best Department of Medical Research, University of Toronto, 112 College Street, Toronto, Ontario M5G 1L6, Canada

Authors and Affiliations

  1. Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, 11724, USA

    George Tokiwa, Mike Tyers, Tom Volpe & Bruce Futcher

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  1. George Tokiwa
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  2. Mike Tyers
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  3. Tom Volpe
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  4. Bruce Futcher
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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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