FIGURE 5.

Drp1 regulates mitochondrial and cardiac dysfunction under HFD treatment. (A) The complex I activity of the wild-type and Drp1 mutant flies under ND or HFD treatment. Two-way ANOVA: Interaction between diet and genotype is significant, p = 0.05. Tukey’s multiple comparison test: *p < 0.05, ns: not significant. N = 5∼6 (5∼6 replicates, 20 flies per replicate). The control group re-uses the data from Figure 2A. (B) The complex IV activity of the wild-type and Drp1 mutant flies under ND or HFD treatment. Two-way ANOVA: Interaction between diet and genotype is not significant, p = 0.8954. Tukey’s multiple comparison test: ns: not significant. N = 9∼10 (9∼10 replicates, 20 flies per replicate). The control group re-uses the date from Figure 2B. (C) The incidence of contractile defects (non-contractile and partial conduction block) of control and Drp1 knockdown flies upon HFD treatment. Chi-square test: Knockdown of Drp1 likely increases the incidence of contractile defects (especially partial conduction block) upon HFD treatment, X ² (1, N = 50) = 7.837, p < 0.01. 15∼20 flies per condition. The control group re-uses the data from Figure 2C. (D) The quantification of the fractional shortening of control and Drp1 knockdown flies. Two-way ANOVA: Interaction between diet and genotype is not significant, p = 0.7507. Tukey’s multiple comparison test: *p < 0.05, **p < 0.01. N = 9∼11 (9∼11 flies per condition). The control group re-uses the data from Figure 2D. (E) The working model showing a novel role of mTORC2 in regulating HFD-induced mitochondrial fission and cardiac dysfunction (created with BioRender.com).