Related Experiment Video
Updated: May 26, 2026

Mitochondrial Respiration Quantification in Yeast Whole Cells
Published on: November 8, 2024
The yeast metacaspase is implicated in oxidative stress response in frataxin-deficient cells
Sophie Lefevre1, Dominika Sliwa, Françoise Auchère
1Mitochondria, 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.
Related Concept Videos
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Caspases
The Intrinsic Apoptotic Pathway
Electron Transport Chain: Complex III and IV
Cellular Injury V: Apoptosis and Autophagy

