IN rapidly growing cells of the budding yeast Saccharomyces cerevisiae, the cell cycle is regulated chiefly at Start, just before the G1-S boundary 1, whereas in the fission yeast Schizosaccharomyces pombe, the cycle is predominantly regulated at G2-M (ref. 2). Both control points are present in both yeasts, and both require the p34cdc2 protein kinase 3-5. At G2-M, p34cdc2 kinase activity in S. pombe requires a B-type cyclin in a complex with p34cdc2 (refs 6-14); this complex is the same as MPF (maturation promoting factor 15,16). The p34cdc2 activity at the G1-S transition in S. cerevisiae may be regulated by a similar cyclin complex, using one of the product of a new class of cyclin genes (CLN1, CLN2 and WHI1 (DAF1/CLN3)) (refs 17-22). At least one is required for progression through the G1-S phase, and deletion of all three leads to G1 arrest 19. WHI1 was isolated as a dominant allele causing budding yeast cells to divide at a reduced size 21 and was later independently identified as DAF1, a dominant allele of which rendered the cells refractory to the G1-arrest induced by the mating pheromone alpha-factor 22. The dominant alleles are truncations thought to yield proteins of increased stability, and the cells are accelerated through G1 (refs 20, 22). Without WHI1 function, the cells are hypersensitive to alpha-factor 22, enlarged and delayed in G1 (refs 20, 22). Heretofore, this G1-class of cyclins has not been identified in other organisms. We have isolated a G1-type cyclin gene called puc1+ from S. pombe, using a functional assay in S. cerevisiae. Expression of puc1+ in S. pombe indicates that it has a cyclin-like role in the fission yeast distinct from the role of the B-type mitotic cyclin.