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Autophagy. 2014 Jun;10(6):1143-5. doi: 10.4161/auto.28767.

A histone point mutation that switches on autophagy.

Author information

1
Institute of Molecular Biosciences; University of Graz; Graz, Austria.
2
INSERM U848; Pavillon de Recherche 1; Villejuif, France; Metabolomics and Cell Biology Platforms; Institut Gustave Roussy; Pavillon de Recherche 1; Villejuif, France; Université Paris Sud, Faculté de Médecine; Le Kremlin Bicêtre; Paris, France.
3
Institute of Molecular Biosciences; University of Graz; Graz, Austria; Division of Endocrinology and Metabolism; Department of Internal Medicine; Medical University of Graz; Graz, Austria.
4
HEALTH-Institute for Biomedicine and Health Sciences; Joanneum Research Forschungsgesellschaft m.b.H.; Graz, Austria.
5
Division of Endocrinology and Metabolism; Department of Internal Medicine; Medical University of Graz; Graz, Austria; HEALTH-Institute for Biomedicine and Health Sciences; Joanneum Research Forschungsgesellschaft m.b.H.; Graz, Austria.
6
Department of Cardiology; Medical University of Graz; Graz, Austria.
7
Department of Dermatology; University Freiburg Medical Center; Freiburg, Germany.
8
Institute for Biology/Genetics; Freie Universität; Berlin, Germany; NeuroCure, Charité; Berlin, Germany.
9
INSERM U848; Pavillon de Recherche 1; Villejuif, France; Metabolomics and Cell Biology Platforms; Institut Gustave Roussy; Pavillon de Recherche 1; Villejuif, France; Université Paris Sud, Faculté de Médecine; Le Kremlin Bicêtre; Paris, France; Equipe 11 Labellisée Ligue Contre le Cancer; INSERM U1138; Centre de Recherche des Cordeliers; Paris, France; Pôle de Biologie; Hôpital Européen Georges Pompidou; AP-HP; Paris, France; Université Paris Descartes; Sorbonne Paris Cité; Paris, France.

Abstract

The multifaceted process of aging inevitably leads to disturbances in cellular metabolism and protein homeostasis. To meet this challenge, cells make use of autophagy, which is probably one of the most important pathways preserving cellular protection under stressful conditions. Thus, efficient autophagic flux is required for healthy aging in many if not all eukaryotic organisms. The regulation of autophagy itself is affected by changing metabolic conditions, but the precise metabolic circuitries are poorly understood. Recently, we found that the nucleocytosolic pool of acetyl-coenzyme A (AcCoA) functions as a major and dominant suppressor of cytoprotective autophagy during aging. Here, we propose an epigenetic mechanism for AcCoA-mediated autophagy suppression that causally involves the regulation of histone acetylation and changes in the autophagy-relevant transcriptome.

KEYWORDS:

ATG; acetyl-coenzyme A; aging; autophagy; epigenetic; histone acetylation; transcription

PMID:
24879160
PMCID:
PMC4091175
DOI:
10.4161/auto.28767
[Indexed for MEDLINE]
Free PMC Article

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