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FEBS Lett. 2012 Jan 20;586(2):143-8. doi: 10.1016/j.febslet.2011.12.002. Epub 2011 Dec 7.

The yeast metacaspase is implicated in oxidative stress response in frataxin-deficient cells.

Author information

1
Mitochondria, Metals and Oxidative Stress Laboratory, Institut Jacques Monod, CNRS-Université Paris-Diderot, Sorbonne Paris Cité, 15 rue Hélène Brion, 75205 Paris Cedex 13, France.

Abstract

Friedreich ataxia is the most common recessive neurodegenerative disease and is caused by reduced expression of mitochondrial frataxin. Frataxin depletion causes impairment in iron-sulfur cluster and heme biosynthesis, disruption of iron homeostasis and hypersensitivity to oxidants. Currently no pharmacological treatment blocks disease progression, although antioxidant therapies proved to benefit patients. We show that sensitivity of yeast frataxin-deficient cells to hydrogen peroxide is partially mediated by the metacaspase. Metacaspase deletion in frataxin-deficient cells results in recovery of antioxidant capacity and heme synthesis. In addition, our results suggest that metacaspase is associated with mitochondrial respiration, intracellular redox control and genomic stability.

PMID:
22155640
DOI:
10.1016/j.febslet.2011.12.002
[Indexed for MEDLINE]
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