Fig. 3. COUP-TFI overexpression in cTG cortical progenitors leads to rostral expansion of MEC and the formation of ectopic MEC.

(A and B) Nissl staining, in situ hybridization, and immunostaining were performed for MEC-enriched genes (A) and NC-enriched genes (B) on P7 sagittal sections of control and cTG (cTG-het; COUP-TFI^TG/+;Emx1-Cre) cortices. The border between NC and MEC (marked by arrowhead) was rostrally shifted in the cTG cortices. Ectopic MEC domains (asterisks) were identified in the caudal NC of cTG. (C to F) Immunostaining of MEC layer markers demonstrates the similar molecular characteristics and layering structure in endogenous MEC from control cortex (C and D) and ectopic MEC from cTG (E and F). (G) DiI crystal was placed at the dorsal hippocampus in P7 control and cTG cortices. DiI-labeled neurons and neuronal processes could be detected in the dorsal MEC (arrowhead) in control and the rostrally expanded MEC (arrowhead) and ectopic MEC (asterisks) in cTG. (H) DiD was placed in the primary visual cortex (V1) in P7 control and cTG cortices, and DiD-labeled neurons and neuronal processes could be detected in the dLG in both control and cTG. DiD-labeled neuronal processes could also be detected in the perforant path (PP, arrows) in the cTG hippocampal formation (Hp). VB, ventrobasal nucleus. Scale bars, 500 μm (A, B, G, and H) and 100 μm (D and F).