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. 2014 Jun 19;3(2):312–323. doi: 10.1016/j.stemcr.2014.05.016

Figure 2.

Figure 2

Alteration of Cell Proliferation and Phenotype in the Adult SEZ/RMS upon Ptc Deletion

(A) Detection of fast proliferating cells by IHF using anti-BrdU antibody in brain slices of Ptc−/− and control animals treated 1 year before with tamoxifen and analyzed 2 hr after short BrdU pulses.

(B) Histogram depicting the number of BrdU+ and GFAP+ cells quantified in the SEZ at the indicated time after tamoxifen treatment.

(C and D) IHF visualizing the expression of EGFR (red) and PSA-NCAM (green) in the SEZ of control and Ptc−/− mice 1 year after tamoxifen administration and quantification.

(E and F) ISH showing the Gfap gene expression in the SEZ of control and Ptc−/− mice 1 year after tamoxifen administration and quantification for the various time points.

(G) Fluorescent micrographs in the adult SEZ of control and Ptc−/− mice 2 months after tamoxifen administration. The micrographs depict immunostainings for GLAST and GFAP/KI67 as astrocyte and stem cell markers, SOX2 and SOX9 as transcription factors necessary for NSC formation, and EGFR and PSA-NCAM as markers of TAPs and migrating neuroblasts, respectively. In the last panels, BrdU labels the fast proliferating cell populations. The dashed lines delineate the wall of the lateral ventricle except for the last two panels on the right where they delineate the cc.

(H) Histograms describing the number of each cell type per square millimeter. Values are the mean ± SEM from three to four animals, two to four slices per animal.

CPu, caudate putamen; LV, lateral ventricle. p ≤ 0.05; ∗∗p ≤ 0.005; ∗∗∗p ≤ 0.0005. Scale bars, 100 μm (A and G), 25 μm (GFAP/KI67 pictures in G), and 50 μm (C and E).

See also Figure S3.