GPR56 Functions Together with α3β1 Integrin in Regulating Cerebral Cortical Development
Figure 1
Dual deletion of Itga3 and Gpr56 results in cortical lamination defect.
(A–D) Nissl staining on coronal sections of P0 Itga3+/−/Gpr56+/− (A), Itga3−/−/Gpr56+/− (B), Itga3+/−/Gpr56−/− (C), and Itga3−/−/Gpr56−/− (D). Normal cortical lamination was observed in Itga3+/−/Gpr56+/− (A) and Itga3−/−/Gpr56+/− (B), while cortical ectopias were seen in Itga3+/−/Gpr56−/− (C) and Itga3−/−/Gpr56−/− (D) brains. (E–H) Higher magnification of boxed regions in A–D. (I–L) Cux1(red) IHC. (M–P) Double IHC of Tbr1 (red) and CTIP2 (green). In contrast to the well organized cortical layers in Itga3+/−/Gpr56+/− brains (I and M), regional overmigration of both superficial and deeper layer neurons were observed in Itga3−/−/Gpr56+/− (J and N), Itga3+/−/Gpr56−/− (K and O), and Itga3−/−/Gpr56−/− (L and P) brains. Scale bars: A–D, 500 µm; E–P, 100 µm.