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. 2022 Jul 15;10:866210. doi: 10.3389/fcell.2022.866210

FIGURE 1.

FIGURE 1

mTORC2 regulates HFD-induced mitochondrial fission in Drosophila hearts. (A) Immunostaining of phospho-Akt in fly cardiomyocytes after 2 days of ND or HFD treatment. Scale bar: 10 μm. (B) The quantification of mean fluorescence intensity of the phospho-Akt. Student’s t-test (*p < 0.05). N = 10 (10 hearts per diet, 2 cardiomyocytes per heart). (C) Western blot analysis of the pAkt, Akt and beta-actin in fly hearts. (D) The quantification of band intensity of the phospho-Akt normalized to total Akt. Student’s t-test (*p < 0.05). N = 3 (3 replicates per diet, 20 hearts per replicate). (E) Immunostaining of mitochondria and F-actin of cardiomyocytes from ND- or HFD-treated control (yw R ) and rictor knockdown flies. The cardiac driver Hand4.2-Gal4 is used to drive heart-specific knockdown. Mitochondria are visualized using an anti-ATP5A1 antibody. Scale bar: 10 μm. Arrows: elongated mitochondria. Arrowheads: fragmented mitochondria. (F) The proportion of the elongated mitochondria with a maximum diameter greater than 2 μm in ND- or HFD-treated control and rictor knockdown flies. Two-way ANOVA: Interaction between diet and genotype is significant, p = 0.0155. Tukey’s multiple comparison test: *p < 0.05, ns: not significant. N = 3∼6 (3∼6 hearts per genotype). (G) The proportion of the elongated mitochondria in hearts with rictor overexpression. Student’s t-test (ns: not significant). N = 3∼6 (3∼6 hearts per genotype).