Overexpression of frataxin in the mitochondria increases resistance to oxidative stress and extends lifespan in Drosophila.
In Friedreich's ataxia, reduction of the mitochondria protein frataxin results in the accumulation of iron and reactive oxygen species, which leads to oxidative damage, neurodegeneration and a diminished lifespan. Recent studies propose that frataxin might play a role in the antioxidative process. Here we show that overexpression of Drosophila frataxin in the mitochondria of female transgenic animals increases antioxidant capability, resistance to oxidative stress insults, and longevity. This suggests that Drosophila frataxin may function to protect the mitochondria from oxidative stresses and the ensuing cellular damage.
Runko
Alexander P
AP
Porter Neuroscience Research Center, MSC 3705, NINDS, NIH, Bethesda, MD 20892, USA.
Griswold
Anthony J
AJ
Min
Kyung-Tai
KT
D000818:Animals; D030801:Animals, Genetically Modified; D000975:Antioxidants; D004331:Drosophila melanogaster / Q000235:genetics / Q000378:metabolism*; D015870:Gene Expression; D005786:Gene Expression Regulation; D033862:Iron-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D008136:Longevity; D008928:Mitochondria / Q000378:metabolism*; D018384:Oxidative Stress; D012333:RNA, Messenger; D000096923:Frataxin
D000975:Antioxidants; D033862:Iron-Binding Proteins; D012333:RNA, Messenger; D000096923:Frataxin