Figure 1: Tsc1 ablation results in OL differentiation and maturation defects. | Nature Communications

Figure 1: Tsc1 ablation results in OL differentiation and maturation defects.

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

Figure 1

(a) Immunostaining for Tsc1 in OPCs (A2B5+), differentiating and maturating OLs (CNP+), terminally differentiated OL (MBP+) induced by treatment with T3 for 0, 1 and 3 days (left to right), respectively. Scale bar, 10 μm. (b) Expression of Tsc1 and Tsc2 assessed by western blot in OPCs treated with T3 for 0, 1 and 3 days. β-actin was used as loading control. (c) Schematic diagram of Cre-mediated excision of the floxed Tsc1 exons 17 and 18, a region of the gene that encodes an essential coiled-coil domain. (d) Expression of Tsc1 and Tsc2 in the corpus callosum of control and Tsc1cKO mice at P14 was examined by western blot. (e) Primary OPCs from control and Tsc1cKO mice were immunostained with antibodies to Tsc1 and Sox10. Scale bar, 10 μm. (f) The optic nerve of Tsc1cKO mice at P12 appears translucent compared with the control. (g–i) Expression of MBP and Plp1 mRNAs was examined by in situ hybridization in the (g,h) cortex and (i) spinal cord of Tsc1cKO and control mice at indicated ages. Scale bar, 100 μm. (j,k) MBP immunostaining in the (j) cerebellum and (k) cerebral cortex of control, and Tsc1cKO at P28 and P67. Scale bar, 100 μm. Arrows indicate white matter tracts. (l) Expression of MBP in the corpus callosum of control and Tsc1cKO mice at P14 was examined by western blot. β-actin was used as loading control.

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