Evidence map›Paper›PMID 34995509›Full record

ArticleMolecular cell2022

Glucose starvation induces a switch in the histone acetylome for activation of gluconeogenic and fat metabolism genes.

Wen-Chuan Hsieh, Benjamin M Sutter, Holly Ruess, Spencer D Barnes, Venkat S Malladi, Benjamin P Tu

Open access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. SIRT1 Exon 2-Encoded IDR Gates CREB-Dependent Transcriptional Timing During Fasting.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  12. Crosstalk BetweenCancers · 2026
    Review
  13. Article
  14. Review
  15. Article
  16. Article
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  18. Article
  19. Review
  20. Article

5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Wen-Chuan HsiehDepartment of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Benjamin M SutterDepartment of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Holly RuessLyda Hill Department of Bioinformatics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Spencer D BarnesLyda Hill Department of Bioinformatics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Venkat S MalladiLyda Hill Department of Bioinformatics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Benjamin P TuDepartment of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX, USA; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: benjamin.tu@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USHoward Hughes Medical Institute · US

Funding

METABOLIC SIGNALS DRIVING CELL GROWTH & PROLIFERATIONR01GM094314 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI TU, BENJAMIN P · 2010 to 2019
$3.2M
Metabolic signals regulating cell growth versus survivalR35GM136370 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI Benjamin P Tu · 2020 to 2026
$2.8M
Targeting Acetyl-CoA Metabolism for the Discovery of New Anti-Cancer TherapeuticsR01CA185169 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MCKNIGHT, STEVEN L, TU, BENJAMIN P · 2014 to 2018
$2.4M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA185169NIGMS NIH HHS R01 GM094314NIGMS NIH HHS R35 GM136370
6 · The paper itself

Abstract

Acetyl-CoA is a key intermediate situated at the intersection of many metabolic pathways. The reliance of histone acetylation on acetyl-CoA enables the coordination of gene expression with metabolic state. Abundant acetyl-CoA has been linked to the activation of genes involved in cell growth or tumorigenesis through histone acetylation. However, the role of histone acetylation in transcription under low levels of acetyl-CoA remains poorly understood. Here, we use a yeast starvation model to observe the dramatic alteration in the global occupancy of histone acetylation following carbon starvation; the location of histone acetylation marks shifts from growth-promoting genes to gluconeogenic and fat metabolism genes. This reallocation is mediated by both the histone deacetylase Rpd3p and the acetyltransferase Gcn5p, a component of the SAGA transcriptional coactivator. Our findings reveal an unexpected switch in the specificity of histone acetylation to promote pathways that generate acetyl-CoA for oxidation when acetyl-CoA is limiting.

Indexed as

GluconeogenesisLipid MetabolismProtein Processing, Post-TranslationalAcetylationAcetyl Coenzyme AGene Expression Regulation, FungalGlucoseHistone AcetyltransferasesHistone DeacetylasesHistonesp300-CBP-Associated FactorSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTrans-ActivatorsAcetyl Coenzyme AGCN5 protein, S cerevisiaeGlucoseHistone AcetyltransferasesHistone DeacetylasesHistonesp300-CBP-Associated FactorRPD3 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSAGA complex, S cerevisiaeTrans-Activatorsacetyl-CoAenvironmental stress responsefat metabolismGcn5pgluconeogenesisglucose starvationhistone acetylationRpd3pSAGAtranscription

Identifiers

PMID34995509
PMCPMC8794035
OpenAlexW4206484283

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.