ArticleProceedings of the National Academy of Sciences of the United States of America2013
Acetyl-CoA induces transcription of the key G1 cyclin CLN3 to promote entry into the cell division cycle in Saccharomyces cerevisiae.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.
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Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Pooled it
- Local acetyl-CoA metabolism and acetate recycling as epigenetic regulators of chromatin dynamics.FEMS yeast research · 2026Review
- Trained Immunity-Like Memory in Vascular Structural Cells: Metabolic-Epigenetic Reprogramming as a Driving Mechanism of Atherosclerosis and Residual Cardiovascular Risk.Journal of inflammation research · 2026Review
- Metabolic expression profiling analysis reveals pyruvate-mediated EPHB2 upregulation promotes lymphatic metastasis in head and neck squamous cell carcinomas.Journal of translational medicine · 2025Article
- Extending the G1 phase improves the production of lipophilic compounds in yeast by boosting enzyme expression and increasing cell size.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Cytoskeletal association of ATP citrate lyase controls the mechanodynamics of macropinocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Two-way communication between cell cycle and metabolism in budding yeast: what do we know?Frontiers in microbiology · 2023Article
- Cell Cycle Progression Influences Biofilm Formation in Saccharomyces cerevisiae 1308.Microbiology spectrum · 2022Article
- Article
- Acetyl-CoA: An interplay between metabolism and epigenetics in cancer.Frontiers in molecular medicine · 2022Review
- ACOT12-mediated acetyl-CoA hydrolysis suppresses intrahepatic cholangiocarcinoma metastasis by inhibiting epithelial-mesenchymal transition.Journal of Cancer · 2022Article
- The Coenzyme A Level Modulator Hopantenate (HoPan) Inhibits Phosphopantotenoylcysteine Synthetase Activity.ACS chemical biology · 2021Article
- Bend or break: how biochemically versatile molecules enable metabolic division of labor in clonal microbial communities.Genetics · 2021Review
- Increased biosynthesis of acetyl-CoA in the yeast Saccharomyces cerevisiae by overexpression of a deregulated pantothenate kinase gene and engineering of the coenzyme A biosynthetic pathway.Applied microbiology and biotechnology · 2021Article
- GCN5 acetyltransferase in cellular energetic and metabolic processes.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- ROS and hypoxia signaling regulate periodic metabolic arousal during insect dormancy to coordinate glucose, amino acid, and lipid metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Metabolic Fuel for Epigenetic: Nuclear Production Meets Local Consumption.Frontiers in genetics · 2021Review
- Cellular quiescence in budding yeast.Yeast (Chichester, England) · 2021Review
- Genome-scale reconstruction of Gcn4/ATF4 networks driving a growth program.PLoS genetics · 2020Article
- Redox controls metabolic robustness in the gas-fermenting acetogenProceedings of the National Academy of Sciences of the United States of America · 2020Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In budding yeast cells, nutrient repletion induces rapid exit from quiescence and entry into a round of growth and division. The G1 cyclin CLN3 is one of the earliest genes activated in response to nutrient repletion. Subsequent to its activation, hundreds of cell-cycle genes can then be expressed, including the cyclins CLN1/2 and CLB5/6. Although much is known regarding how CLN3 functions to activate downstream targets, the mechanism through which nutrients activate CLN3 transcription in the first place remains poorly understood. Here we show that a central metabolite of glucose catabolism, acetyl-CoA, induces CLN3 transcription by promoting the acetylation of histones present in its regulatory region. Increased rates of acetyl-CoA synthesis enable the Gcn5p-containing Spt-Ada-Gcn5-acetyltransferase transcriptional coactivator complex to catalyze histone acetylation at the CLN3 locus alongside ribosomal and other growth genes to promote entry into the cell division cycle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.