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| Subject Categories: Signal Transduction | Cellular Metabolism |
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| The EMBO Journal
(2005) 24, 4271–4278, doi:10.1038/sj.emboj.7600889 Published online 24 November 2005 |
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| Regulation of G0 entry by the Pho80–Pho85 cyclin–CDK complex |
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| Valeria Wanke1, Ivo Pedruzzi1, Elisabetta Cameroni1, Frédérique Dubouloz and Claudio De Virgilio |
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Department of Microbiology and Molecular Medicine, CMU, University of Geneva, Geneva, Switzerland To whom correspondence should be addressed Claudio De Virgilio, Department of Microbiology & Molecular Medicine, CMU, University of Geneva, 1211 Geneva, Switzerland. Tel.: +41 22 379 54 95; Fax: +41 22 379 55 02; E-mail: Claudio.DeVirgilio@medecine.unige.ch 1 These authors contributed equally to this work Received 12 August 2005; Accepted 4 November 2005; Published online 24 November 2005. |
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| Abstract |
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| Eukaryotic cell proliferation is controlled by growth factors and essential nutrients. In their absence, cells may enter into a quiescent state (G0). In Saccharomyces cerevisiae, the conserved protein kinase A (PKA) and rapamycin-sensitive TOR (TORC1) pathways antagonize G0 entry in response to carbon and/or nitrogen availability primarily by inhibiting the PAS kinase Rim15 function. Here, we show that the phosphate-sensing Pho80–Pho85 cyclin–cyclin-dependent kinase (CDK) complex also participates in Rim15 inhibition through direct phosphorylation, thereby effectively sequestering Rim15 in the cytoplasm via its association with 14-3-3 proteins. Inactivation of either Pho80–Pho85 or TORC1 causes dephosphorylation of the 14-3-3-binding site in Rim15, thus enabling nuclear import of Rim15 and induction of the Rim15-controlled G0 program. Importantly, we also show that Pho80–Pho85 and TORC1 converge on a single amino acid in Rim15. Thus, Rim15 plays a key role in G0 entry through its ability to integrate signaling from the PKA, TORC1, and Pho80–Pho85 pathways. |
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| Keywords: G0, nutrient starvation, Pho80–Pho85 cyclin–CDK complex, Rim15, TORC1 |
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