Figure 3: Hyperactivation of mTOR signalling contributes to dysmyelination in Tsc1 mutants. | Nature Communications

Figure 3: Hyperactivation of mTOR signalling contributes to dysmyelination in Tsc1 mutants.

From: Regulation of PERK–eIF2α signalling by tuberous sclerosis complex-1 controls homoeostasis and survival of myelinating oligodendrocytes

Figure 3

(a) Representative images of the corpus callosum of control and Tsc1cKO mutants treated with vehicle and rapamycin from P5 to P14 immunostained with p-S6 and CC1. Scale bar, 50 μm. (b) Lysates of control and Tsc1cKO corpus callosum at P14 assayed by western blot using antibodies to MBP, p-mTOR, p-S6 and S6. β-actin was used as loading control. (c) The number of CC1+ cells per mm2 from the corpus callosum of control and Tsc1cKO mice-treated vehicle and rapamycin. Data represent the mean±s.e.m from four animals per genotype. *P<0.05; **P<0.01; *** P<0.001, One-way analysis of variance (ANOVA) with Tukey's multiple-comparison test. (d) The corpus callosum of control and Tsc1cKO mutants at P14-treated vehicle and rapamycin from P5 to P14 was immunostained with MBP. Scale bar, 100 μm. (e) Percentage of MBP area in the cortex of control and Tsc1cKO mice treated with vehicle or rapamycin. Data represent the mean±s.e.m from four animals per genotype. *P<0.05; **P<0.01; ***P<0.001. One-way ANOVA with Tukey's multiple-comparison test. (f) OPCs isolated from control and Tsc1cKO mice were cultured in the differentiation medium for 24 h with vehicle and rapamycin, and immunostained with GalC and p-S6. Scale bar, 50 μm. (g) The percentage of GalC+ cells in cultures of control and Tsc1cKO OPCs. Data represent the mean±s.e.m. from three independent experiments. *P<0.05; **P<0.01; ***P<0.001. One-way ANOVA with Tukey's multiple-comparison test.

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