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


Journal

Life science alliance
ISSN: 2575-1077
Titre abrégé: Life Sci Alliance
Pays: United States
ID NLM: 101728869

Informations de publication

Date de publication:
02 2019
Historique:
received: 29 10 2018
revised: 28 01 2019
accepted: 29 01 2019
entrez: 10 2 2019
pubmed: 10 2 2019
medline: 10 2 2019
Statut: epublish

Résumé

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.

Identifiants

pubmed: 30737248
pii: 2/1/e201800228
doi: 10.26508/lsa.201800228
pmc: PMC6369536
pii:
doi:

Substances chimiques

DNA, Mitochondrial 0
Histones 0
Ketoglutaric Acids 0
Acetyl Coenzyme A 72-89-9
Histone Acetyltransferases EC 2.3.1.48
DNA Polymerase gamma EC 2.7.7.7
POLG protein, human EC 2.7.7.7
Acetate-CoA Ligase EC 6.2.1.1
Dinoprostone K7Q1JQR04M

Types de publication

Journal Article Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2019 Lozoya et al.

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Auteurs

Oswaldo A Lozoya (OA)

Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.

Tianyuan Wang (T)

Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.

Dagoberto Grenet (D)

Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.

Taylor C Wolfgang (TC)

Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.

Mack Sobhany (M)

Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.

Douglas Ganini da Silva (D)

Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA.

Gonzalo Riadi (G)

Centro de Bioinformática y Simulación Molecular, Facultad de Ingeniería, Universidad de Talca, Talca, Chile.

Navdeep Chandel (N)

Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL.

Richard P Woychik (RP)

Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA rick.woychik@nih.gov.

Janine H Santos (JH)

Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC, USA janine.santos@nih.gov.

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Classifications MeSH