Fig. 7: Tcf4 restoration in the Foxg1 cKO CGE rescued the pallial PROX1⁺ CIN fate.

a Immunostaining of anti-PROX1, anti-ST18, in situ hybridization of Erbb4 at E16.5 and in situ hybridization of Tcf4 at E15.5 (from Allen Brain Atlas, http://developingmouse.brain-map.org/experiment/show/100051538) showing high expression in the MGE and the dLGE/CGE (arrows) but low expression in the vLGE (arrowheads) in control mice (the experiments were repeated independently at least three times with similar results). While this unique expression pattern of PROX1 and ST18 was disrupted in Foxg1 cKO mice (yellow arrows). b Genome browser view of FOXG1 CUT&Tag data at the Tcf4 locus in the wild type GE cells (WT-Anti FOXG1: treated with FOXG1 antibody, WT-Negative Control: without FOXG1 antibody) and Foxg1 cKO GE cells (treated with FOXG1 antibody). Shadow showing FOXG1-binding position on the Tcf4 locus. Bar plots showing the activation of FOXG1 at the Tcf4 promoter site detected by luciferase assay (n = 3 replicates of the luciferase assay). Data are presented as means ± SEM. Two-tailed unpaired t test; ***P  <  0.001, ****P  <  0.0001; pCAG-FOXG1 vs. pCAG: ***P = 0.0009. Source data are provided as a Source Data file. c Double immunostaining of anti-mCherry with PROX1 at E16.5 and quantification analysis of the number of mCherry⁺PROX1⁺ CINs in Foxg1 cKO cortex at E16.5 (n = 3 mice in pCAGIG-mCherry group, n = 4 mice in pCAGIG-mTcf4-cDNA-mCherry group), showing that Tcf4 restoration in the Foxg1 cKO CGE rescued the pallial CIN fate. Arrows: mCherry and PROX1 co-expressed pallial CINs. Data are presented as means ± SEM. Two-tailed unpaired t test; ***P  <  0.001, ****P  <  0.0001; pCAGIG-mTcf4-cDNA-mCherry vs. pCAGIG-mCherry: ***P = 0.0003. Source data are provided as a Source Data file.