Fig. 2.

Genetic deletion of PcdhγC4 increased cell death in MGE-derived cINs. (A) Diagram of genetic crosses between MGE/POA-specific reporter and Pcdhγ^C4KO mice. Pcdhγ^C4KO homozygous MGE cells were obtained from the Nkx2.1^Cre;Ai14;Pcdhγ^C4KO/C4KO embryos, whereas control cells were obtained from Nkx2.1^Cre;Ai6 embryos. (B) Schematics of transplantation protocol. The MGEs from E13.5 Pcdhγ^C4KO homozygous mutant or control embryos were dissected, dissociated, and mixed in similar proportions. The mixture of GFP⁺ (Pcdhγ^WT) and tdTomato⁺ (Pcdhγ^C4KO/C4KO) cells was grafted into the cortex of WT neonate mice. (C) Left—Confocal images from the cortex of mice at 6 and 21 DAT. The transplanted cells are labeled with GFP (Pcdhγ^WT) or tdTomato (Pcdhγ^C4KO/C4KO). Right—Quantifications (shown as survival fraction) of surviving MGE-derived cINs at 6 and 21 DAT. Both the transplanted GFP and tdTomato-labeled cells undergo PCD between 6 and 21 DAT, but the Pcdhγ^C4KO/C4KO cells are eliminated at significantly higher rates. (D) Survival fraction quantifications from (C) shown by individual brain sections (each bar) and separated by animals at 6 and 21 DAT. Scale bar = 50 μm, nested ANOVA, ****P =3.147e-10, n = 5 mice per time point and 10 brain sections quantified per mouse, DAT 6 cells counted = 9,125, DAT 21 cells counted = 3,125.