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Fig. 8 | BMC Biology

Fig. 8

From: orsai, the Drosophila homolog of human ETFRF1, links lipid catabolism to growth control

Fig. 8

osi loss of function produces a metabolic defect not rescued by antioxidants. A Mitochondrial ATP levels normalized to total protein. Three independent samples were evaluated. Two-tailed t-test was performed. B Mitostress analysis shows a reduction in oxygen consumption (OCR) in osi mutants at 72h AEL. Data was normalized to the number of larvae. Two independent samples were evaluated. C Glycostress analysis reveals a reduced glycolytic metabolism in osi mutants as well as an altered response to glucose intake at 72h AEL. Data was normalized to the number of larvae. Six independent samples were examined. D Dihydroethidium (DHE) was employed to detect ROS by fluorescence microscopy in 24h AEL larvae. Animals from 2 different plates were used. The total number of fat bodies analyzed are indicated. A two-tailed t-test was performed. E Sod2 expression in osi-depleted animals using actG4. Three independent samples were taken into account. A one-way ANOVA with Bonferroni’s multiple comparisons was performed. The total number of animals per condition is indicated. F Addition of the antioxidant NAC to the food did not improve survival of osi-depleted animals. The experiment was repeated twice. All panels: different letters indicate significant differences, p<0.05; treatments displaying the same letter (alone or in combination) are not statistically different. A Shapiro-Wilk test was used for normality assessment (see Additional file 2). The total number of samples analyzed is described below the corresponding panel. All datasets and statistical analysis on which the conclusions are based are included in Additional file 2

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