Overexpression of Human and Fly Frataxins in Drosophila Provokes Deleterious Effects at Biochemical, Physiological and Developmental Levels
Figure 4
Molecular effects of frataxin overexpression and the involvement of oxidative stress.
(A) The negative effects of human-frataxin overexpression on aconitase activity under normoxia and hyperoxia (99.5% O2) conditions. (B) Human frataxin overexpression triggered a reduction in the synthesis of the complex I subunit (amount normalized to the internal control α-tubulin). (C–E) Increased susceptibility to hyperoxia-mediated oxidative damage in flies overexpressing human and fly frataxin in the nervous system. (F,G) Constitutive expression of mitochondrial catalase (mitoCat) led to an extension of the mean and maximum life span of the flies with increased frataxin expression. This effect was strong in the peripheral nervous system (neur-GAL4) and moderate in the glial cells (repo-GAL4). (H) Co-expression of mitochondrial catalase (mitoCat) rescues (5d) and alleviates (10d) the locomotor deficits in the flies with an increased level of frataxin expression in the glial cells. The survival curves were analyzed using the Kapplan-Meier test. The level of significance in A, B and H was determined using a one-way ANOVA with a post hoc Newman-Keuls test (*p<0.05). The error bars represent the standard error.