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. Author manuscript; available in PMC: 2017 Feb 27.
Published in final edited form as: Nat Neurosci. 2009 Oct 4;12(11):1390–1397. doi: 10.1038/nn.2408

Figure 3.

Figure 3

GSK-3 deletion in progenitors strongly inhibits neurogenesis. (a) Marked thinning of cortical areas filled with Tuj1-positive cells in Gsk3a−/−; Gsk3bloxP/loxP; nestin-cre brain sections at E13.5. Scale bar represents 500 μm. (b) This was also observed with Tbr1, a deeper- layer neuron marker, staining. Scale bar represents 50 μm. (c) NeuN-positive neurons were also markedly less frequent in Gsk3a−/−; Gsk3bloxP/loxP; nestin-cre cortical sections. Scale bar represents 100 μm. (d) Quantification of Tuj1-, Sox2-, Tbr1- and NeuN-positive cells. The ratios of Tuj1-, Sox2- and Tbr1-positive cells to the DAPI-stained cells per field were measured and shown as relative change versus control. Relative changes of NeuN-positive areas in Gsk3a−/−; Gsk3bloxP/loxP; nestin-cre tissue samples were scored by measuring NeuN-positive areas with ImageJ software. n = 10 sections from each of three mutant and control embryos per each condition. * P < 0.01. (e) Western blotting showed that the neuronal makers Tuj1, MAP2, SMI32 and NeuN were downregulated in Gsk3a−/−; Gsk3bloxP/loxP; nestin-cre brain tissues. However, the progenitor markers Nestin and Pax6 were upregulated. Tissue lysates from three mutant and control brains per each condition were used. (f) Quantification of western blot data. We used three independent blots from each condition for quantification.