Control of G1 cyclin expression in Saccharomyces cerevisiae is mediated primarily by the transcription factor SBF (Swi4/Swi6). In the absence of Swi4 and Swi6 cell viability is lost, but can be regained by ectopic expression of the G1 cyclin encoding genes, CLN1 or CLN2. Here we demonstrate that the RME1 (regulator of meiosis) gene can also bypass the normally essential requirement for SBF. RME1 encodes a zinc finger protein which is able to repress transcription of IME1 (inducer of meiosis) and thereby inhibit cells from entering meiosis. We have found that expression of RME1 from a high copy number plasmid can specifically induce CLN2 expression. Deletion of RME1 alone shows no discernible effect on vegetative growth, however, deletion of RME1 in a swi6 delta swi4ts strain results in a lowering of the non-permissive temperature for viability. This suggests that Rme1 plays a significant but ancillary role in SBF in inducing CLN2 expression. We show that Rme1 interacts directly with the CLN2 promoter and have mapped the region of the CLN2 promoter required for Rme1-dependent activation. Consistent with Rme1 having a cell cycle role in G1, we have found that RME1 mRNA is synthesized periodically in the cell cycle, with maximum accumulation occurring at the M/G1 boundary. Thus Rme1 may act both to promote mitosis, by activating CLN2 expression, and prevent meiosis, by repressing IME1 expression.