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Altered lipid metabolism in a Drosophila model of Friedreich's ataxia

Friedreich’s ataxia (FRDA) is the most common form of autosomal recessive ataxia caused by a deficit in the mitochondrial protein frataxin. Although demyelination is a common symptom in FRDA patients, no multicellular model has yet been developed to study the involvement of glial cells in FRDA. Using the recently established RNAi-lines for targeted suppression of frataxin in Drosophila, we were able to study the effects of general versus glial specific frataxin downregulation. In particular we wanted to study the interplay between lowered frataxin content, lipid accumulation and peroxidation and the consequences of these effects on the sensitivity to oxidative stress and fly fitness.

Altered lipid metabolism in a Drosophila model of Friedreich's ataxia

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