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[Preprint]. 2023 Feb 6:2023.02.03.526887. [Version 2] doi: 10.1101/2023.02.03.526887

Figure 3 -. Most MGE-derived cINs survive the deletion of most Pcdhγ, except for Pcdhγc4.

Figure 3 -

A. Diagram of genetic crosses between MGE/POA-specific reporter Nkx2.1Cre;Ai14 and Pcdhγ1R1 mice. Control cells were derived from Nkx2.1Cre;Ai6 mice while Pcdhγ1R1 mutant cells were derived from Nkx2.1Cre;Ai14; Pcdhγ1R1/1R1 mice.

B. Diagram of the transplantation protocol. The MGEs from E13.5 Pcdhγ1R1 homozygous or control embryos were dissected, dissociated, and mixed in similar proportions. The mixture of GFP+ (PcdhγWT) and tdTomato+ (Pcdhγ1R1/1R1) cells was grafted into the cortex of WT neonate mice.

C. Left - Confocal images from the cortex of 6 and 21 DAT mice. The transplanted cells are labeled with GFP (PcdhγWT) or tdTomato (Pcdhγ1R1/1R1). Right - Quantifications of the transplanted cells that survived at 6 and 21 DAT. Note that both the GFP or tdTomato labeled cells underwent programmed cell death between 6 and 21 DAT, but both cell types survived to similar levels.

D. Survival fraction quantification from (C) shown by the brain section (each bar) and separated by animals at 6 and 21 DAT.

Scale bar = 50 um, Nested-ANOVA, ***p = 0.0026, n = 4 mice per time point and 10 brain sections per mouse.