Yeast G1 cyclins are unstable in G1 phase

Brandt L. Schneider, E. Elizabeth Patton, Stefan Lanker, Michael D. Mendenhall, Curt Wittenberg, Bruce Futcher and Mike Tyers ()
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Brandt L. Schneider: Cold Spring Harbor Laboratory
E. Elizabeth Patton: Programme in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital
Stefan Lanker: The Scripps Research Institute
Michael D. Mendenhall: Markey Cancer Center, Dept. of Biochemistry, University of Kentucky
Curt Wittenberg: The Scripps Research Institute
Bruce Futcher: Cold Spring Harbor Laboratory
Mike Tyers: Programme in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital

Nature, 1998, vol. 395, issue 6697, 86-89

Abstract: Abstract In most eukaryotes, commitment to cell division occurs in late G1 phase at an event called Start in the yeast Saccharomyces cerevisiae1, and called the restriction point in mammalian cells2. Start is triggered by the cyclin-dependent kinase Cdc28 and threerate-limiting activators, the G1 cyclins Cln1, Cln2 and Cln3 (ref. 3). Cyclin accumulation in G1 is driven in part by the cell-cycle-regulated transcription of CLN1 and CLN2, which peaks at Start3. CLN transcription is modulated by physiological signals that regulate G1 progression4,5, but it is unclear whether Cln protein stability is cell-cycle-regulated. It has been suggested that once cells pass Start, Cln proteolysis is triggered by the mitotic cyclins Clb1, 2, 3 and 4 (ref. 6). But here we show that G1 cyclins are unstable in G1 phase, and that Clb–Cdc28 activity is not needed for G1 cyclin turnover. Cln instability thus provides a means to couple Cln–Cdc28 activity to transcriptional regulation and protein synthetic rate in pre-Start G1 cells.

Date: 1998
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DOI: 10.1038/25774

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