Evidence map›Paper›PMID 33253182›Full record

ArticlePLoS biology2020

Acetylation-mediated remodeling of the nucleolus regulates cellular acetyl-CoA responses.

Ryan Houston, Shiori Sekine, Michael J Calderon, Fayaz Seifuddin, Guanghui Wang, Hiroyuki Kawagishi, Daniela A Malide, Yuesheng Li, Marjan Gucek, Mehdi Pirooznia and 8 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 35 citations in OpenAlex.

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  18. Vitamin BNature metabolism · 2023
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 4 institutions in 1 country.

Ryan HoustonAging Institute, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0001-9494-2514
Shiori SekineAging Institute, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Michael J CalderonDepartment of Cell Biology, Center for Biologic Imaging, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0002-0820-7888
Fayaz SeifuddinNational Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, United States of America.
Guanghui WangNational Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, United States of America.
Hiroyuki KawagishiNational Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, United States of America.ORCID 0000-0001-7622-341X
Daniela A MalideNational Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, United States of America.
Yuesheng LiNational Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, United States of America.
Marjan GucekNational Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, United States of America.
Mehdi PiroozniaNational Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, United States of America.ORCID 0000-0002-4210-6458
Alissa J NelsonCell Signaling Technology, INC., Danvers, Massachusetts, United States of America.ORCID 0000-0003-3622-6944
Matthew P StokesCell Signaling Technology, INC., Danvers, Massachusetts, United States of America.
Jacob Stewart-OrnsteinDepartment of Computational and Systems Biology, University of Pittsburgh and Hillman Cancer Center, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0001-8255-5904
Steven J MullettDepartment of Pharmacology and Chemical Biology, the Health Sciences Metabolomics and Lipidomics Core, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Stacy G WendellDepartment of Pharmacology and Chemical Biology, the Health Sciences Metabolomics and Lipidomics Core, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0001-9083-6933
Simon C WatkinsDepartment of Cell Biology, Center for Biologic Imaging, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0003-4092-1552
Toren FinkelAging Institute, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Yusuke SekineAging Institute, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID 0000-0003-0345-1416
University of Pittsburgh · USNational Heart Lung and Blood Institute · USCell Signaling Technology (United States) · USUPMC Hillman Cancer Center · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
Vascular autophagy as a mediator of vascular aging and homeostasisR01HL142663 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FINKEL, TOREN · 2018 to 2021
$2.2M
Defining and manipulating quiescence associated DNA damage resistance in single cellsR00CA207727 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STEWART-ORNSTEIN, JACOB · 2019 to 2021
$735k
Bringing Untargeted Metabolomics to PittS10OD023402 · OD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GELHAUS, STACY LYNN · 2018 to 2018
$594k
NCI NIH HHS P30 CA047904NCI NIH HHS R00 CA207727NHLBI NIH HHS R01 HL142663NIH HHS S10 OD023402
6 · The paper itself

Abstract

The metabolite acetyl-coenzyme A (acetyl-CoA) serves as an essential element for a wide range of cellular functions including adenosine triphosphate (ATP) production, lipid synthesis, and protein acetylation. Intracellular acetyl-CoA concentrations are associated with nutrient availability, but the mechanisms by which a cell responds to fluctuations in acetyl-CoA levels remain elusive. Here, we generate a cell system to selectively manipulate the nucleo-cytoplasmic levels of acetyl-CoA using clustered regularly interspaced short palindromic repeat (CRISPR)-mediated gene editing and acetate supplementation of the culture media. Using this system and quantitative omics analyses, we demonstrate that acetyl-CoA depletion alters the integrity of the nucleolus, impairing ribosomal RNA synthesis and evoking the ribosomal protein-dependent activation of p53. This nucleolar remodeling appears to be mediated through the class IIa histone deacetylases (HDACs). Our findings highlight acetylation-mediated control of the nucleolus as an important hub linking acetyl-CoA fluctuations to cellular stress responses.

Indexed as

AcetatesAcetylationAcetyl Coenzyme AATP Citrate (pro-S)-LyaseCell LineCell NucleolusGene ExpressionGene Knockout TechniquesHCT116 CellsHistone DeacetylasesHumansModels, BiologicalNuclear ProteinsProtein Processing, Post-TranslationalRibosomal ProteinsTumor Suppressor Protein p53AcetatesAcetyl Coenzyme AATP Citrate (pro-S)-LyaseHistone DeacetylasesNuclear ProteinsRibosomal ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID33253182
PMCPMC7728262
OpenAlexW3108112326

What OpenQuestion holds

Textmetadata
LicenceCC0
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.