Yeast G1 cyclins are unstable in G1 phase

被引:58
|
作者
Schneider, BL
Patton, EE
Lanker, S
Mendenhall, MD
Wittenberg, C
Futcher, B
Tyers, M
机构
[1] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
[2] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Programme Mol Biol & Canc, Toronto, ON M5G 1X5, Canada
[3] Univ Toronto, Grad Dept Mol & Med Genet, Toronto, ON M5S 1A8, Canada
[4] Scripps Res Inst, Dept Mol Biol, La Jolla, CA 92037 USA
[5] Univ Kentucky, Dept Biochem, Lucille P Markey Canc Ctr, Lexington, KY 40536 USA
关键词
D O I
10.1038/25774
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
In most eukaryotes, commitment to cell division occurs in late G1 phase at an event called Start in the yeast Saccharomyces cerevisiae(1), and called the restriction point in mammalian cells(2). Start is triggered by the cyclin-dependent kinase Cdc28 and three rate-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 Start(3). CLN transcription is modulated by physiological signals that regulate G1 progression(4,5), 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.
引用
收藏
页码:86 / 89
页数:4
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