期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2004
卷号：101
期号：16
页码：6086-6091
DOI：10.1073/pnas.0308314101
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：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 Ca2+-sensitive phenotypes of the zds1{Delta} strain, such as the Ca2+-induced, Swe1p- and Cln2p-mediated G2 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 Ca2+ sensitivity by the sah1-1 mutation. Exogenous AdoMet transiently led the cells to G1 cell-cycle 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.
