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. 2010 Apr 5;30(11):2737–2749. doi: 10.1128/MCB.01566-09

FIG. 3.

FIG. 3.

Defective OPC development in CK2βloxP/loxP, Nestin-cre telencephalons. (A) Schematic of a coronal telencephalon section. The green and red boxes indicate the regions analyzed for the detection of parenchymal OPCs in panel B and of ventral OPCs in panel C, respectively. (B) Analysis of NG2 (green) and PECAM (red) expressions by immunohistochemistry (IHC) in E18.5 wild-type and CK2βloxP/loxP, Nestin-cre telencephalons. Note the normal appearance of multiprocessed NG2+ parenchymal OPCs in the wild type and their absence in CK2βloxP/loxP, Nestin-cre embryos. The pattern of NG2 staining in vessel pericytes parallels PECAM endothelial cell labeling (yellow) and was unaffected. (C) NG2 and PECAM expression analysis (IHC) revealed the presence of ventral NG2+ OPCs (arrowheads) in CK2βloxP/loxP, Nestin-cre fetal (E14.5) and late embryonic (E16.5 to E18.5) telencephalons. (D) In situ hybridization (ISH) analysis of Pdgfra expression in fetal (E14.5) and late embryonic (E16.5 to E18.5) telencephalons. There was a significant reduction (***, P values of 2.5 × 10−10 at E16.5 and 1.0 × 10−6 at E18.5 [4 embryos per dpc and per genotype and 3 nonadjacent sections per telencephalon]) of Pdgfra+ OPCs in CK2βloxP/loxP, Nestin-cre telencephalons compared to the number in wild-type controls. lv, lateral ventricle. Scale bars, 100 μm (B and C) and 200 μm (D).