Acetyl-CoA induces transcription of the key G1 cyclin CLN3 to promote entry into the cell division cycle in Saccharomyces cerevisiae

Shi, Lei; Tu, Benjamin P.

doi:10.1073/pnas.1302490110

Cited by 129Fungal and yeast genetics researchGenomics and Chromatin DynamicsGene Regulatory Network Analysis

Acetyl-CoA induces transcription of the key G1 cyclin CLN3 to promote entry into the cell division cycle in Saccharomyces cerevisiae

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Shi, Lei, Tu, Benjamin P.·2013·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.1302490110PMC PMC3645525

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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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Histone acetylation is exquisitely sensitive to alterations in cellular nutritional and signaling status.
“Histone acetylation is exquisitely sensitive to alterations in the cellular nutritional and signaling status (Cai et al., 2011; Shi and Tu, 2013).”
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Authors: Shi, L., & Tu, B. P.
Affiliations: The University of Texas Southwestern Medical Center (US)
ORCID: Shi, Lei
Tu, Benjamin P.
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2013-04-15
Volume: 110
Issue: 18
Pages: 7318-7323
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.1302490110
PMC: PMC3645525
OpenAlex: W2008892277
Cited by: 129
References: 75
Citations by year: 2026: 4 · 2025: 2 · 2024: 4 · 2023: 5 · 2022: 7 · 2021: 7 · 2020: 10 · 2019: 17 · 2018: 12 · 2017: 10 · 2016: 11 · 2015: 22 · 2014: 14 · 2013: 4
FWCI: 7.61
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of General Medical Sciences (R01GM094314)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gene Regulatory Network Analysis
Keywords: acetyl-CoA, CLN3, G1 cyclins, histone acetylation, GCN5, transcriptional activation, quiescence exit, cell cycle entry, glucose catabolism, Saccharomyces cerevisiae
MeSH terms: Acetyl Coenzyme A, Acetylation, Cell Cycle, Glucose, Histones, Models, Biological, Promoter Regions, Genetic, Ribosomal Proteins, Saccharomyces cerevisiae, Transcription, Genetic, Trans-Activators, Gene Expression Regulation, Fungal, Cyclins, Saccharomyces cerevisiae Proteins, Multiprotein Complexes, Cyclin G1

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Acetyl-CoA induces transcription of the key G1 cyclin CLN3 to promote entry into the cell division cycle in Saccharomyces cerevisiae

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