Biotin starvation causes mitochondrial protein hyperacetylation and partial rescue by the SIRT3-like deacetylase Hst4p
| Autor: | Martin Hey-Mogensen, Michael Lisby, Jon W. Poulsen, Sara Larsen, Michael L. Nielsen, Jonas T. Treebak, Kathrine B. Sylvestersen, Marianne A. Andersen, Eva Maria Akke Palmqvist, Christian Madsen, Clifford Young, Per B. Jensen |
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| Přispěvatelé: | Madsen, Christian T, Sylvestersen, Kathrine B, Young, Clifford, Larsen, Sara C, Poulsen, Jon W, Andersen, Marianne A, Palmqvist, Eva A, Hey-Mogensen, Martin, Jensen, Per B, Treebak, Jonas T, Lisby, Michael, Nielsen, Michael L |
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
General Physics and Astronomy
Mitochondrion Mass Spectrometry chemistry.chemical_compound 0302 clinical medicine Biotin Homeostasis 2. Zero hunger chemistry.chemical_classification 0303 health sciences Multidisciplinary biology Hst4p Acetylation Biotin starvation mitochondrial Mitochondria Biochemistry Sirtuin Niacinamide Saccharomyces cerevisiae Proteins SIRT3 Cellular respiration Cell Respiration Biotin deficiency Saccharomyces cerevisiae Article Histone Deacetylases General Biochemistry Genetics and Molecular Biology Mitochondrial Proteins 03 medical and health sciences Oxygen Consumption Acetyl Coenzyme A medicine 030304 developmental biology Reactive oxygen species Organisms Genetically Modified General Chemistry NAD medicine.disease Microscopy Fluorescence chemistry Starvation biology.protein Hst4p deacetylase Energy Metabolism Reactive Oxygen Species 030217 neurology & neurosurgery |
| Zdroj: | Madsen, C T, Sylvestersen, K B, Young, C, Larsen, S C, Poulsen, J W, Andersen, M A, Palmqvist, E A, Hey-Mogensen, M, Jensen, P B, Treebak, J T, Lisby, M & Nielsen, M L 2015, ' Biotin starvation causes mitochondrial protein hyperacetylation and partial rescue by the SIRT3-like deacetylase Hst4p ', Nature Communications, vol. 6, 7726 . https://doi.org/10.1038/ncomms8726 Nature Communications |
| DOI: | 10.1038/ncomms8726 |
| Popis: | The essential vitamin biotin is a covalent and tenaciously attached prosthetic group in several carboxylases that play important roles in the regulation of energy metabolism. Here we describe increased acetyl-CoA levels and mitochondrial hyperacetylation as downstream metabolic effects of biotin deficiency. Upregulated mitochondrial acetylation sites correlate with the cellular deficiency of the Hst4p deacetylase, and a biotin-starvation-induced accumulation of Hst4p in mitochondria supports a role for Hst4p in lowering mitochondrial acetylation. We show that biotin starvation and knockout of Hst4p cause alterations in cellular respiration and an increase in reactive oxygen species (ROS). These results suggest that Hst4p plays a pivotal role in biotin metabolism and cellular energy homeostasis, and supports that Hst4p is a functional yeast homologue of the sirtuin deacetylase SIRT3. With biotin deficiency being involved in various metabolic disorders, this study provides valuable insight into the metabolic effects biotin exerts on eukaryotic cells. Biotin is an essential vitamin in the regulation of energy metabolism. Here Madsen et al. show that biotin deficiency in yeast leads to hyperacetylation of mitochondrial proteins that is compensated for by the SIRT-like deacetylase Hst4p. |
| Databáze: | OpenAIRE |
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