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. 2020 Jul 11;88(4):688–702. doi: 10.1002/ana.25833

FIGURE 1.

FIGURE 1

Generation of a mouse model overexpressing the Sod1 G86R transgene but lacking all subcerebral projection neurons (SubCerPN), including the corticospinal neurons (CSN). (A) Schematic diagram of the crossbreeding of the Sod1 G86R and Fezf2 −/− mouse lines to generate four genotypes of interest: WT, KO, Sod1, and KO/Sod1. (B) Retrograde labeling of the CSN from the spinal cord of KO animals (right) and WT (left), showing absence of CSN in KO mice. n = 5 for all genotypes. (C) Representative images of brain coronal sections, at the level of the motor cortex, showing CTIP2 immunolabeling of layer V SubCerPN and of layer VI corticothalamic projection neurons (CThPN) in WT and Sod1 mice, and confirming the absence of cortical layer V SubCerPN from the KO and KO/Sod1 animals. n = 3 for all genotypes. (D) Quatitative PCR analysis of Fezf2, Sod1, and Chat expression in the cerebral cortex and spinal cord of 75‐day‐old animals, indicating that absence of Fezf2 does not affect Sod1 or Chat expression; 2‐way ANOVA; n = 4 WT, n = 4 KO, n = 4 Sod1, and n = 2 KO/Sod1; ***p < 0.001. Scale bars: 400μm in upper panels and 200μm in lower panels of B; and 250μm in C. [Color figure can be viewed at www.annalsofneurology.org]