S-adenosyl-L-methionine (AdoMet) is a molecule central to general metabolism, serving as a principal methyl donor for methylation of various cellular constituents. The alteration in the availability of AdoMet has profound effect on cell growth. A mutant allele of Saccharomyces cerevisiae gene SAH1 encoding S-adenosyl-L-homocysteine (AdoHcy) hydrolase, was isolated as a mutation that suppressed the Ca 2؉ -sensitive phenotypes of the zds1⌬ strain, such as the Ca 2؉ -induced, Swe1p-and Cln2p-mediated G 2 cell-cycle arrest, and polarized bud growth. The mutation (sah1-1) led the cells to accumulate AdoMet besides AdoHcy, the substrate of Sah1p. The cells treated with exogenous AdoMet and AdoHcy had markedly decreased levels of SWE1 and CLN2 mRNA, providing the basis for the suppression of the Ca 2؉ sensitivity by the sah1-1 mutation. Exogenous AdoMet transiently led the cells to G1 cellcycle delay whereas AdoHcy caused growth inhibition irrelevant to the cell cycle. The effect of AdoMet in inducing the cell-cycle delay was exerted in a manner independent of Met4p, an overall transcriptional activator for MET genes. Our observation provides an insight into the role played by AdoMet in cell cycle regulation. E ukaryotic cells coordinate cell growth in response to a variety of external signals. In the budding yeast Saccharomyces cerevisiae, commitment to a new round of cell duplication occurs at a control point called Start. Execution of Start demands a sufficient level of G 1 cyclin͞Cdc28 protein kinase activity and is a requirement for DNA synthesis, bud formation, and replication of the spindle pole body (1).Unger and Hertwell (2) found that sulfate starvation of a prototroph, methionine starvation of an auxotroph, or a shift of a conditional methionyl-tRNA synthetase mutant to a restrictive condition led to arrest in G 1 . They proposed that the signal for the nutrients was generated at the level of protein biosynthesis. It was recently shown that disruption of the gene for MET30, an E3 ubiquitin ligase, caused the arrest of G 1 (3). MET30 is an essential gene that encodes a negative regulator of the sulfur amino acid biosynthesis pathway (4, 5). The uncontrolled accumulation of Met4p, a transcriptional activator for MET genes (6), in a met30⌬ strain has been suggested to inhibit passage of Start by preventing the accumulation of G 1 transcripts, such as CLN1 and CLN2 (3). It is therefore reasonable to expect some sort of connection between the cyclin-Cdc28p kinase complex and several external signals, including nutrient signals, although the underlying mechanisms are not completely known (7).L-methionine is an essential amino acid required for protein synthesis and participates, together with ATP, in the formation of S-adenosylmethionine (AdoMet). AdoMet is a high-energy sulfonium compound that is used in the majority of biological methylation reactions (7, 8). On demethylation, AdoMet is converted into S-adenosylhomocysteine (AdoHcy), a molecule that can be further hydrolyzed to adenosine and homocysteine by AdoH...

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