TORC1 controls G1-S cell cycle transition in yeast via Mpk1 and the greatwall kinase pathway
- Moreno-Torres, Marta Department of Biology, University of Fribourg, Switzerland
- Jaquenoud, Malika Department of Biology, University of Fribourg, Switzerland
- De Virgilio, Claudio Department of Biology, University of Fribourg, Switzerland
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10.09.2015
Published in:
- Nature Communications. - 2015, vol. 6, p. 8256
English
The target of rapamycin complex 1 (TORC1) pathway couples nutrient, energy and hormonal signals with eukaryotic cell growth and division. In yeast, TORC1 coordinates growth with G₁–S cell cycle progression, also coined as START, by favouring the expression of G₁ cyclins that activate cyclin-dependent protein kinases (CDKs) and by destabilizing the CDK inhibitor Sic1. Following TORC1 downregulation by rapamycin treatment or nutrient limitation, clearance of G₁ cyclins and C-terminal phosphorylation of Sic1 by unknown protein kinases are both required for Sic1 to escape ubiquitin-dependent proteolysis prompted by its flagging via the SCFCdc4 (Skp1/Cul1/F-box protein) ubiquitin ligase complex. Here we show that the stabilizing phosphorylation event within the C-terminus of Sic1 requires stimulation of the mitogen-activated protein kinase, Mpk1, and inhibition of the Cdc55 protein phosphatase 2A (PP2ACdc55) by greatwall kinase-activated endosulfines. Thus, Mpk1 and the greatwall kinase pathway serve TORC1 to coordinate the phosphorylation status of Sic1 and consequently START with nutrient availability.
- Faculty
- Faculté des sciences et de médecine
- Department
- Département de Biologie
- Language
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- English
- Classification
- Biological sciences
- License
- License undefined
- Identifiers
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- RERO DOC 257048
- DOI 10.1038/ncomms9256
- Persistent URL
- https://folia.unifr.ch/unifr/documents/304548
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