Skip to main content
. 2018 Oct 11;29(9):3738–3751. doi: 10.1093/cercor/bhy253

Figure 7.

Figure 7.

Radial migration of Sadb-deficient neurons is not impaired. (A) Immunostaining of Sadb wild-type (+/+, left) and homozygous (−/−, right) cerebral cortex at P0 with layer-specific markers. Cux1 (II–IV layer marker, red, upper panels), Ctip2 (Vb–VI layer marker, green, middle panels) staining, and their overlay (lower panels). Bar: 50 μm. (B) Confirmation of Sadb−/− brains. Lysates of the cerebral cortex of Sadb wild-type (+/+), heterozygous (+/−), and homozygous (−/−) mutant mice at P0 were analyzed by immunoblotting using the indicated antibodies. (C) In utero electroporation. pCAGGS-EGFP vector was electroporated into the cerebral cortices at E14.5, followed by fixation at P0. The brain sections were immunostained with anti-GFP (green), anti-Ctip2 (red) antibody, and DAPI (blue). Representative images of the staining of wild-type (+/+, left) and homozygous (−/−, right) brains. CP, cortical plate, IZ, intermediate zone. Bar, 50 μm. (D) Quantification of the distribution of GFP-positive cells in 4 distinct parts of the cerebral cortex (bins 1–4 as indicated in the inset) of Sadb+/+ (closed bars, n = 5) or Sadb−/− (open bars, n = 5) mice. Data are expressed as means ± SEM. There were no significant differences between the 2 groups (bin 4, P = 0.850; bin 3, P = 0.333; bin 2, P = 0.054; bin 1, P = 0.927).