Fig. 4: Activation of REPTOR in wildtype muscle increases glucose content and promotes myofiber degradation.
From: REPTOR and CREBRF encode key regulators of muscle energy metabolism
a Protein levels of REPTOR measured from thoraces. N = 2 biologically independent samples. Results were reproduced in three independent experiments. Numbers indicate densitometry of bands normalized to control. b Glucose content in thoraces (Ctrl vs REPTOR[WT] p = 0.74 ns, Ctrl vs REPTOR[WT] + PRAS40 p < 0.0001****, Ctrl vs REPTOR[WT] + Tsc1/Tsc2 p < 0.0001****). N = 12 biologically independent samples, N = 8 thoraces per sample. Results were reproduced in three independent experiments. c Percentage of thoraces showing myofiber degradation (p < 0.0001****). Total number of hemi-thoraces scored for each genotype is shown. d–g Immunostaining of the flight muscles of control (d), REPTOR[WT] (e), or REPTOR[WT] co-expressed with PRAS40 (f) or Tsc1/Tsc2 (g). Myofibrils were labelled with phalloidin (magenta) and mitochondria with CoxIV (green). Gene expression was induced for 8 days (b–g) Data shows mean with ±SD (b). Values were normalized to the mean of control samples (b). Statistical analysis was done by using one-way ANOVA with Sidak correction test for multiple comparisons (b), or two-tailed Fisher’s exact test with a confidence interval of 95% for pairwise comparisons between two groups (c). Scale bar is 5 µm in (d–g). Source data are provided as a Source Data file.
