A Saccharomyces cerevisiae strain unable to store neutral lipids is tolerant to oxidative stress induced by α-synuclein.
Identifieur interne : 000A49 ( PubMed/Checkpoint ); précédent : 000A48; suivant : 000A50A Saccharomyces cerevisiae strain unable to store neutral lipids is tolerant to oxidative stress induced by α-synuclein.
Auteurs : Yves Y. Sere [France] ; Matthieu Regnacq ; Jenny Colas ; Thierry BergesSource :
- Free radical biology & medicine [ 1873-4596 ] ; 2010.
English descriptors
- KwdEn :
- Adaptation, Biological (drug effects), Adaptation, Biological (genetics), Drug Resistance (genetics), Enzyme Activation (drug effects), Fatty Acid Synthases (metabolism), Glutathione (metabolism), Lipid Metabolism (genetics), Lipid Metabolism Disorders (genetics), Lipid Metabolism Disorders (pathology), Models, Theoretical, Organisms, Genetically Modified, Oxidation-Reduction (drug effects), Oxidative Stress (drug effects), Oxidative Stress (genetics), Oxidative Stress (physiology), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae (metabolism), Squalene (metabolism), alpha-Synuclein (genetics), alpha-Synuclein (metabolism), alpha-Synuclein (pharmacology), alpha-Synuclein (physiology).
- MESH :
- chemical , genetics : alpha-Synuclein.
- chemical , metabolism : Fatty Acid Synthases, Glutathione, Squalene, alpha-Synuclein.
- drug effects : Adaptation, Biological, Enzyme Activation, Oxidation-Reduction, Oxidative Stress.
- genetics : Adaptation, Biological, Drug Resistance, Lipid Metabolism, Lipid Metabolism Disorders, Oxidative Stress, Saccharomyces cerevisiae.
- growth & development : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- pathology : Lipid Metabolism Disorders.
- chemical , pharmacology : alpha-Synuclein.
- physiology : Oxidative Stress, alpha-Synuclein.
- Models, Theoretical, Organisms, Genetically Modified.
Abstract
Parkinson disease is a neurodegenerative pathology that has been linked to several genetic mutations of the SNCA gene encoding the pro-oxidant α-synuclein protein. The budding yeast Saccharomyces cerevisiae is a valuable model for studying the cellular and molecular mechanisms of α-synuclein toxicity. Indeed heterologous expression of α-synuclein is toxic to wild-type yeast and exhibits the main features of damage caused to mammalian neurons, including an increase in neutral lipid storage (triglycerides and steryl esters, embedded into lipid droplets). To address the significance of this accumulation, we forced α-synuclein production in a strain unable to synthesize triglycerides and steryl esters. Surprisingly, the inability to store neutral lipids rendered the cells more tolerant to α-synuclein. Our results indicate that the level of α-synuclein toxicity is correlated with fatty acid synthase activity and intracellular redox status.
DOI: 10.1016/j.freeradbiomed.2010.09.007
PubMed: 20850523
Affiliations:
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pubmed:20850523Le document en format XML
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<front><div type="abstract" xml:lang="en">Parkinson disease is a neurodegenerative pathology that has been linked to several genetic mutations of the SNCA gene encoding the pro-oxidant α-synuclein protein. The budding yeast Saccharomyces cerevisiae is a valuable model for studying the cellular and molecular mechanisms of α-synuclein toxicity. Indeed heterologous expression of α-synuclein is toxic to wild-type yeast and exhibits the main features of damage caused to mammalian neurons, including an increase in neutral lipid storage (triglycerides and steryl esters, embedded into lipid droplets). To address the significance of this accumulation, we forced α-synuclein production in a strain unable to synthesize triglycerides and steryl esters. Surprisingly, the inability to store neutral lipids rendered the cells more tolerant to α-synuclein. Our results indicate that the level of α-synuclein toxicity is correlated with fatty acid synthase activity and intracellular redox status.</div>
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<Abstract><AbstractText>Parkinson disease is a neurodegenerative pathology that has been linked to several genetic mutations of the SNCA gene encoding the pro-oxidant α-synuclein protein. The budding yeast Saccharomyces cerevisiae is a valuable model for studying the cellular and molecular mechanisms of α-synuclein toxicity. Indeed heterologous expression of α-synuclein is toxic to wild-type yeast and exhibits the main features of damage caused to mammalian neurons, including an increase in neutral lipid storage (triglycerides and steryl esters, embedded into lipid droplets). To address the significance of this accumulation, we forced α-synuclein production in a strain unable to synthesize triglycerides and steryl esters. Surprisingly, the inability to store neutral lipids rendered the cells more tolerant to α-synuclein. Our results indicate that the level of α-synuclein toxicity is correlated with fatty acid synthase activity and intracellular redox status.</AbstractText>
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