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Oxidative stress induces mitochondrial fragmentation in frataxin-deficient cells.

Authors
  • Sophie Lefevre
  • Dominika Sliwa
  • Pierre Rustin
  • Jean-Michel Camadro
  • Renata Santos
Identifiers
DOI: 10.1016/j.bbrc.2012.01.022
Source
CdV-UPMC
License
Unknown

Abstract

Friedreich ataxia (FA) is the most common recessive neurodegenerative disease. It is caused by deficiency in mitochondrial frataxin, which participates in iron-sulfur cluster assembly. Yeast cells lacking frataxin (Δyfh1 mutant) showed an increased proportion of fragmented mitochondria compared to wild-type. In addition, oxidative stress induced complete fragmentation of mitochondria in Δyfh1 cells. Genetically controlled inhibition of mitochondrial fission in these cells led to increased resistance to oxidative stress. Here we present evidence that in yeast frataxin-deficiency interferes with mitochondrial dynamics, which might therefore be relevant for the pathophysiology of FA. Copyright © 2012 Elsevier Inc. All rights reserved.

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