Figure 8

Nfib -deficient mice exhibit callosal dysgenesis. (A-H) Carbocyanine tract tracing in wildtype (A, B, E, F) and Nfib mutant (C, D, G, H) brains at E18. DiI was injected into the neocortex of wildtype and knockout brains, thereby labelling all neocortical projections, including the CC. In the wildtype at rostral (A, B) and caudal (E, F) levels, callosal axons were seen projecting across the midline (arrows in (B, F)). In the knockout at rostral levels, no axons were observed crossing the midline (arrowhead in (D)). However, at more caudal levels, a small number of axons were seen crossing into the contralateral cortex (arrow in (H)). (I-P) Immunohistochemistry against the axonal marker GAP43 in wildtype (I, J, M, N) and Nfib mutant (K, L, O, P) brains at E18. The CC was clearly observed in the wildtype at rostral and caudal levels (arrows in (J, N)). In the mutant at rostral levels, no GAP43-positive axons were seen crossing the midline. Instead, axons stopped adjacent to the midline (arrowheads in (L)). More caudally, however, a small CC was evident in the mutant (arrow in (P)). Panels (B, D, F, H, J, L, N, P) are higher magnifications of the boxed regions in (A, C, E, G, I, K, M, O), respectively. Scale bars: 500 μm (A, C, E, G, I, K, M, O); 200 μm (B, D, F, H, J, L, N, P).