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 esse ntial for G(1) progression past Start, but until now its regulation ha s been poorly understood. Here we show that the cig2/cyc17 B-type cycl in has an important role in G(1) progression, and demonstrate that p34 (cdc2) kinase activity is periodically associated with cig2 in G(1). C ells lacking cig2 are defective in G(1) progression, and this is parti cularly 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) p rogression, Whilst p25(rum1) can inhibit cig2/cdc2 activity in vitro, and may transiently inhibit this complex in vivo, cig1 is regulated in dependently of p25(rum1). Since cig1/cdc2 kinase activity peaks in mit otic cells, and decreases after mitosis with similiar kinetics to cdc1 3-associated kinase activity, we suggest that cig2 is likely to be the principal fission yeast G(1) cyclin, cig2 protein levels accumulate i n G(1) cells, and we propose that p25(rum1) may transiently inhibit ci g2-associated p34(cdc2) activity until the critical cell size required for Start is reached.