Fig. 5: REPTOR sustained activation in muscle represses glycolysis and collapses the energy metabolism program.

a, b Levels of glycolytic metabolites (Glucose-6-P p = 0.0196*, Fructose-6-P p = 0.0068**, Fructose 1,6-bisP p = 0.0042**, Glyceraldehyde-3-P p = 0.0224*, 1,3-Bisphosphoglycerate p = 0.66 ns) (a), or Acetyl-CoA (p = 0.0172*) (b) quantified by LC/MS in thoraces. N = 5 biologically independent samples, N = 45 thoraces per sample. c ATP content in thoraces (p < 0.0001****). N = 8 biologically independent samples, N = 4 thoraces per sample. Results were reproduced in three independent experiments. d Percentage of hemi-thoraces showing myofiber degradation (p < 0.0001****). Total number of hemi-thoraces scored for each genotype is shown. e Levels of TCA cycle metabolites quantified by LC/MS in thoraces as in (a, b) (Oxaloacetate p = 0.0002***, Citrate p = 0.0021**, Isocitrate p = 0.55 ns, alpha-ketoglutarate p = 0.0334*, Succinyl-CoA p = 0.075 ns, Succinate p = 0.0044**, Fumarate p = 0.0112*, Malate p = 0.0027**). N = 5 biologically independent samples, N = 45 thoraces per sample. f Percentage of hemi-thoraces showing myofiber degradation (p < 0.0001****). Total number of hemi-thoraces scored for each genotype is shown. g Model of the function of REPTOR in muscles. ImpL2 promotes REPTOR expression. REPTOR activity represses glucose usage in muscle, while likely promoting the use of lipids as an alternative fuel substrate. REPTOR sustained activation in muscle collapses the energy metabolism program. Data shows boxplots (median and quartiles) with whiskers (minimum to maximum) (a–c, e). All values were normalized to the mean of control samples (a–c, e). Statistical analysis was done using two-tailed t-test with Welch’s correction (a–c, e), or two-tailed Fisher’s exact test with a confidence interval of 95% for pairwise comparisons between two groups (d, f). Source data are provided as a Source Data file.