ArticleProceedings of the National Academy of Sciences of the United States of America2004
Involvement of S-adenosylmethionine in G1 cell-cycle regulation in Saccharomyces cerevisiae.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Analysis of the response mechanism in lipid degradation of key gene LDH1 knockout strains of Saccharomyces cerevisiae under levulinic acid stress.Archives of microbiology · 2025Article
- The Swi-Snf chromatin remodeling complex mediates gene repression through metabolic control.Nucleic acids research · 2023Article
- Article
- Mutations in the S-Adenosylmethionine Synthetase GenesGenetics · 2019Article
- A Benchtop Approach To Measuring S-AdenosylMethionine Metabolite Levels Using HILIC UPLC-MS.Journal of the Kentucky Academy of Science · 2019Article
- Geotrichum candidum gene expression and metabolite accumulation inside the cells reflect the strain oxidative stress sensitivity and ability to produce flavour compounds.FEMS yeast research · 2019Article
- Flexible model-based clustering of mixed binary and continuous data: application to genetic regulation and cancer.Nucleic acids research · 2017Article
- Stimulating S-adenosyl-l-methionine synthesis extends lifespan via activation of AMPK.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Physiological and toxic effects of purine intermediate 5-amino-4-imidazolecarboxamide ribonucleotide (AICAR) in yeast.The Journal of biological chemistry · 2011Article
- GAP promoter library for fine-tuning of gene expression in Pichia pastoris.Applied and environmental microbiology · 2011Article
- S-adenosyl-L-homocysteine hydrolase, key enzyme of methylation metabolism, regulates phosphatidylcholine synthesis and triacylglycerol homeostasis in yeast: implications for homocysteine as a risk factor of atherosclerosis.The Journal of biological chemistry · 2008Article
- Pathways change in expression during replicative aging in Saccharomyces cerevisiae.The journals of gerontology. Series A, Biological sciences and medical sciences · 2008Article
- Diversity of Ca2+-induced morphology revealed by morphological phenotyping of Ca2+-sensitive mutants of Saccharomyces cerevisiae.Eukaryotic cell · 2007Article
- Involvement of calcineurin-dependent degradation of Yap1p in Ca2+-induced G2 cell-cycle regulation in Saccharomyces cerevisiae.EMBO reports · 2006Article
- Transcriptional response of Saccharomyces cerevisiae to desiccation and rehydration.Applied and environmental microbiology · 2005Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 zds1Delta 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 G(1) 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.
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