Journal
YEAST
Volume 35, Issue 3, Pages 281-290Publisher
WILEY
DOI: 10.1002/yea.3296
Keywords
melatonin; mitochondria biogenesis; -synuclein
Categories
Funding
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [302935/2014-2]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [2011/07366-5, 2013/079378, 2011/03583-1]
Ask authors/readers for more resources
One of the hallmarks of Parkinson disease is -synuclein aggregate deposition that leads to endoplasmic reticulum stress, Golgi fragmentation and impaired energy metabolism with consequent redox imbalance. In the last decade, many studies have used Saccharomyces cerevisiae as a model in order to explore the intracellular consequences of -synuclein overexpression. In this study we propose to evaluate the respiratory outcome of yeast cells expressing -synuclein. Cell viability or growth on selective media for respiratory activity was mainly affected in the -synuclein-expressing cells if they were also treated with menadione, which stimulates reactive oxygen species production. We also tested whether melatonin, a natural antioxidant, would counteract the deleterious effects of -synuclein and menadione. In fact, melatonin addition improved the respiratory growth of -synuclein/menadione-challenged cells, presented a general improvement in the enzymatic activity of the respiratory complexes and finally elevated the rate of mitophagy, an important cellular process necessary for the clearance of damaged mitochondria. Altogether, our data confirms that -synuclein impairs respiration in yeast, which can be rescued by melatonin addition.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available