B-type cyclins regulate G(1) progression in fission yeast in opposition to the p25(rum1) cdk inhibitor

The onset of S phase in fission yeast is regulated at Start, the point of commitment to the mitotic cell cycle. The p34(cdc2) kinase is essential for G(1) progression past Start, but until now its regulation has been poorly understood. Here we show that the cig2/cyc17 B-type cyclin has an important role in G(1) progression, and demonstrate that p34(cdc2) kinase activity is periodically associated with cig2 in G(1). Cells lacking cig2 are defective in G(1) progression, and this is particularly clear in small cells that must regulate Start with respect to cell size. We also find that the cig1 B-type cyclin can promote G(1) progression, Whilst p25(rum1) can inhibit cig2/cdc2 activity in vitro, and may transiently inhibit this complex in vivo, cig1 is regulated independently of p25(rum1). Since cig1/cdc2 kinase activity peaks in mitotic cells, and decreases after mitosis with similiar kinetics to cdc13-associated kinase activity, we suggest that cig2 is likely to be the principal fission yeast G(1) cyclin, cig2 protein levels accumulate in G(1) cells, and we propose that p25(rum1) may transiently inhibit cig2-associated p34(cdc2) activity until the critical cell size required for Start is reached.