Acetyl-CoA induces cell growth and proliferation by promoting the acetylation of histones at growth genes
Open accessAbstract
The decision by a cell to enter a round of growth and division must be intimately coordinated with nutrient availability and its metabolic state. These metabolic and nutritional requirements, and the mechanisms by which they induce cell growth and proliferation, remain poorly understood. Herein, we report that acetyl-CoA is the downstream metabolite of carbon sources that represents a critical metabolic signal for growth and proliferation. Upon entry into growth, intracellular acetyl-CoA levels increase substantially and consequently induce the Gcn5p/SAGA-catalyzed acetylation of histones at genes important for growth, thereby enabling their rapid transcription and commitment to growth. Thus, acetyl-CoA functions as a carbon-source rheostat that signals the initiation of the cellular growth program by promoting the acetylation of histones specifically at growth genes.
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Regulation of cytosolic acetyl-CoA generation can modulate transcriptional outputs by altering global histone acetylation.
“Thus, regulation of cytosolic acetyl-CoA generation can modulate transcriptional outputs by altering global histone acetylation (187).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [187]
Citrate export to the cytosol and subsequent cleavage by ACL provides a major source of cytosolic acetyl-CoA that is the obligate substrate for both de novo lipid synthesis and protein acetylation reactions.
“However, citrate export to the cytosol and subsequent cleavage by ACL provides a major source of cytosolic acetyl-CoA that is the obligate substrate for both de novo lipid synthesis and protein acetylation reactions (39, 187, 188).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [187]
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).”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Cai et al., 2011
Peak levels of acetyl-CoA are accompanied by histone acetylation at specific regions of chromatin containing growth genes.
“Peak levels of acetyl-CoA are accompanied by histone acetylation at specific regions of chromatin containing growth genes.”
From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Cai et al., 2011
A rise in intracellular acetyl-CoA occurs in phase with induction of growth genes, and a bolus of extracellular nutrients convertible to acetyl-CoA causes yeast cells to short-circuit the metabolic cycle and enter directly into growth.
“A rise in intracellular acetyl-CoA occurs in phase with the induction of growth genes, and a bolus of extracellular nutrients that can be readily converted to acetyl-CoA causes cells to short-circuit the metabolic cycle and enter directly into growth (Cai et al., 2011).”
From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Cai et al., 2011
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“Thus, regulation of cytosolic acetyl-CoA generation can modulate transcriptional outputs by altering global histone acetylation (187).”
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- Authors
- Cai, L., Sutter, B. M., Li, B., & Tu, B. P.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Tu, Benjamin P.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2011-05
- Volume
- 42
- Issue
- 4
- Pages
- 426-437
- ISSN
- 1097-2765 (ISSN-L)
- PMC
- PMC3109073
- OpenAlex
- W1977622464
- Cited by
- 701
- References
- 52
- Citations by year
- 2026: 29 · 2025: 43 · 2024: 45 · 2023: 44 · 2022: 44 · 2021: 60 · 2020: 53 · 2019: 63 · 2018: 61 · 2017: 48 · 2016: 51 · 2015: 47 · 2014: 43 · 2013: 36 · 2012: 23
- FWCI
- 14.43
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 844 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Texas Southwestern Medical Center
- National Institute of General Medical Sciences (R01GM090077, R01GM094314)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- acetyl-CoA, histone acetylation, GCN5, SAGA complex, cell growth, cell proliferation, nutrient availability, transcriptional activation, growth-related genes, metabolic regulation of gene expression
- MeSH terms
- p300-CBP-Associated Factor, Acetyl Coenzyme A, Acetylation, Histones, Saccharomyces cerevisiae, Signal Transduction, Trans-Activators, Saccharomyces cerevisiae Proteins, Cell Proliferation, Histone Acetyltransferases
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