Evidence map›Paper›PMID 30737248›Full record

ArticleLife science alliance2019

Mitochondrial acetyl-CoA reversibly regulates locus-specific histone acetylation and gene expression.

Oswaldo A Lozoya, Tianyuan Wang, Dagoberto Grenet, Taylor C Wolfgang, Mack Sobhany, Douglas Ganini da Silva, Gonzalo Riadi, Navdeep Chandel, Richard P Woychik, Janine H Santos

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Mitochondria - the CEO of the cell.Journal of cell science · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. The role of lipids in genome integrity and pluripotency.Biochemical Society transactions · 2024
    Review
  14. An Overview: The Diversified Role of Mitochondria in Cancer Metabolism.International journal of biological sciences · 2023
    Review
  15. Mitochondrial signal transduction.Cell metabolism · 2022
    Review
  16. Emerging mitochondrial signaling mechanisms in cardio-oncology: beyond oxidative stress.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  17. Article
  18. Article
  19. Mitochondrial DNA damage as driver of cellular outcomes.American journal of physiology. Cell physiology · 2022
    Review
  20. Article
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

10 authors at 3 institutions in 2 countries.

Oswaldo A LozoyaGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.
Tianyuan WangGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.
Dagoberto GrenetGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.
Taylor C WolfgangGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.
Mack SobhanyGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.
Douglas Ganini da SilvaImmunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.
Gonzalo RiadiCentro de Bioinformática y Simulación Molecular, Facultad de Ingeniería, Universidad de Talca, Talca, Chile.
Navdeep ChandelDepartment of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL.
Richard P WoychikGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA rick.woychik@nih.gov.ORCID 0000-0001-8196-1732
Janine H SantosGenome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA janine.santos@nih.gov.ORCID 0000-0001-6384-3070
National Institutes of Health · USNorthwestern University · USUniversity of Talca · CL

Funding

Gene Expression and MicroarraysZICES102445 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$31.6M
Role of environmental agents targeting mitochondria in epigenetic regulation of nuclear gene expressionZIAES103186 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WOYCHIK, RICHARD · 2014 to 2020
$4.9M
The broad impact of environmental exposures on repetitive element expression in cellular biologyZIAES103187 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WOYCHIK, RICHARD · 2014 to 2020
$3.6M
6 · The paper itself

Abstract

The impact of mitochondrial dysfunction in epigenetics is emerging, but our understanding of this relationship and its effect on gene expression remains incomplete. We previously showed that acute mitochondrial DNA (mtDNA) loss leads to histone hypoacetylation. It remains to be defined if these changes are maintained when mitochondrial dysfunction is chronic and if they alter gene expression. To fill these gaps of knowledge, we here studied a progressive and a chronic model of mtDNA depletion using biochemical, pharmacological, genomics, and genetic assays. We show that histones are primarily hypoacetylated in both models. We link these effects to decreased histone acetyltransferase activity unrelated to changes in ATP citrate lyase, acetyl coenzyme A synthetase 2, or pyruvate dehydrogenase activities, which can be reversibly modulated by altering the mitochondrial pool of acetyl-coenzyme A. Also, we determined that the accompanying changes in histone acetylation regulate locus-specific gene expression and physiological outcomes, including the production of prostaglandins. These results may be relevant to the pathophysiology of mtDNA depletion syndromes and to understanding the effects of environmental agents that lead to physical or functional mtDNA loss.

Indexed as

Acetate-CoA LigaseAcetylationAcetyl Coenzyme ADinoprostoneDNA, MitochondrialDNA Polymerase gammaEpigenesis, GeneticGene ExpressionGenetic LociHEK293 CellsHistone AcetyltransferasesHistonesHumansKetoglutaric AcidsMitochondriaPromoter Regions, GeneticAcetate-CoA LigaseAcetyl Coenzyme ADinoprostoneDNA, MitochondrialDNA Polymerase gammaHistone AcetyltransferasesHistonesKetoglutaric AcidsPOLG protein, human

Identifiers

PMID30737248
PMCPMC6369536
OpenAlexW2883257411

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.