Fig 2: Expression of BCL11B in HRGECs transfected with the miR-650 mimic, mock or inhibitor. (A) The expression of BCL11B was determined by immunofluorescence analysis. (B) Western blot analysis was performed to measure the protein expression of caspase-8 and BCL11B. BCL11B, B-cell CLL/lymphoma 11B; HRGEC, human renal glomerular endothelial cell; miR, microRNA.

Fig 3: Tle4 is required perinatally to maintain CThPN identity during thalamic innervation(A–B′) Fezf2 ISH and CTIP2 immunolabeling (C–E) in Ntsr1-Cre:tdTomatofl:Tle4fl/fl mice.(B′ and B″) Ntsr1-Cre expression limit between somatosensory and motor cortices (white arrow). Magnified insets from boxed areas in low-magnification images. (F and H) SCPN labeling approach by FB injection into pyramidal tract (P3). Analysis (P7) in somatosensory cortex.(G–I) Presence of SCPN (FB+) in LVI and LVex in Ntsr1-Cre:tdTomatofl:Tle4fl/fl mutants, but not in tdTomatofl:Tle4fl/fl controls.(J) Distribution of SCPN (FB+) across cortical thickness; n = 4 mice per genotype. Mean FB+ cells/bin ± SEM; ANOVA-Tukey, **p < 0.01.(K and L) In Ntsr1-Cre:tdTomatofl:Tle4fl/fl mice, reprogrammed SCPN (tdTomato+-FB+ in LVex and LVI) upregulate CTIP2 (solid arrowheads) and downregulate FOG2 (open arrowheads).(M–O) Quantification of tdTomato+ axons from Ntsr1-Cre-expressing neurons in pyramidal tract at P28 (n = 3 per genotype, unpaired t test, **p < 0.01). Error bars, SEM.Scale bars, 500 μm (A–D); 250 μm (G and I); 20 μm (E′–E″′, K, L, and M′); 1 mm (M).

Fig 4: Gene and Protein Expression for Bcll11b.(A) Gene expression for Bcl11b in control striatal STHdh cells (CTL, open bars) and HPRT-knockdown (HPRTKD, closed bars). Bars represent mean ±SEM (n = 4). mRNA expression is normalized to GAPDH RNA level (*P<0.05, t-test). (B) Immuno-blot and quantification of Bcl11b protein expression in striatal cells. The quantification bar graphs are shown as means ± SEM (n = 3, *P<0.05, t-test). (C) Gene expression of Actn2, Arpp19, Foxp1, Ngef, Pde10a, and Rgs9 in control (CTL, open bars) and HPRT knockdown (HPRTKD, closed bars) striatal STHdh cells. Bars represent mean ±SEM (n = 4). *P<0.05, t-test. (D) Gene expression for Bcl11b in the striatum of wild-type (WT, open bars) and HPRT knockout (HPRTKO, closed bars) mice. Bars represent mean ±SEM (n = 4). mRNA expression is normalized to GAPDH RNA level (*P<0.05, t-test). (E) Immuno-blot and quantification of Bcl11b protein expression in the striatum of WT and HPRTKO mice. The quantification bar graphs are shown as means ± SEM (n = 3, *P<0.05, t-test). (F) Gene expression for Actn2, Arpp19, Foxp1, Ngef, Pde10a, and Rgs9 in control (Wild-type, open bars) and HPRT knockout mice (HPRTKO, closed bars) striatum. Bars represent mean ±SEM (n = 4). *P<0.05, t-test.

Fig 5: Brain regions analyzed. Coronal, thionin-stained, hemi-sections of the cerebral hemisphere at the level of the (A) frontal, (B) parietal, (C) temporal, and (D) occipital lobe. Cerebral cortex (Cx; regions outside the dashed line) was examined for all histological and immunohistochemical analysis. Measurements were made in the cerebral cortex (squares indicate fields of view; 4 bins analyzed per square for NeuN; 3 bins analyzed per square for Ctip2; whole square without bins analyzed for SST). A total of 6 fields of view was analyzed from the striatum, with 3 fields of view selected from the caudate nucleus and 3 fields from the putamen (B). Cx, cortex; CC, corpus callosum; Hi, hippocampus; St, striatum; SVZ, subventricular zone; CN, caudate nucleus; Pu, putamen; MB, midbrain.