Fig. 1
Reciprocal expression of COUP-TFI and Foxg1 in the developing neocortex. a Calibrated enrichment probability for Foxg1 expression across cortical layers in the adult mouse somatosensory cortex (http://genserv.anat.ox.ac.uk). b Schematic diagram showing the strategy of Foxg1 expression manipulation by doxycycline administration. In the absence of doxycycline, tet-transactivator (tTA) protein binds to tetO promoter to activate Foxg1 transgene expression. In the presence of doxycycline, doxycycline binds to tTA protein to prevent the activation of transgenic Foxg1 expression. c Schematic diagram showing the timing of doxycycline administration and the corresponding Foxg1 expression. Samples were collected at indicated time points shown in closed arrowheads. d Hierarchical clustering using the complete linkage method with Euclidean distance. Heatmap represents the gene cluster that exhibited rapid expression downregulation upon Foxg1 induction by doxycycline administration. e–e″ Complementary expression of Foxg1 mRNA (green) by in situ hybridization and COUP-TFI protein (red) immunohistochemistry in E15.5 mouse cortex. Dashed lines indicate the ventricular surface. f–j″ Developmental expression of COUP-TFI (red) and Foxg1 (green) in E11.5 (f–f″), E13.5 (g–g″), E15.5 (h–h″), P1 (i–i″), and P4 (j–j″) wild-type cortices. Mouse anti-COUP-TFI (Perseus) and Rabbit anti-Foxg1 (TaKaRa) antibodies were used. Embryonic tissues were processed at the identical condition using cryosections and postnatal tissues were perfused prior to fixation using floating sections. Dashed lines indicate the ventricular surface. VZ ventricular zone, IZ intermediate zone, CP cortical plate, MZ marginal zone, DL deep layer
