In most eukaryotes, commitment to cell division occurs in late G1 phas
e at an event called Start in the yeast Saccharomyces cerevisiae(1), a
nd called the restriction point in mammalian cells(2). Start is trigge
red by the cyclin-dependent kinase Cdc28 and three rate-limiting activ
ators, the G1 cyclins Cln1, Cln2 and Cln3 (ref. 3). Cyclin accumulatio
n in G1 is driven in part by the cell-cycle-regulated transcription of
CLN1 and CLN2, which peaks at Start(3). CLN transcription is modulate
d by physiological signals that regulate G1 progression(4,5), but it i
s unclear whether Cln protein stability is cell-cycle-regulated It has
been suggested that once cells pass Start, Cln proteolysis is trigger
ed 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 p
rotein synthetic rate in pre-Start G1 cells.