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. Author manuscript; available in PMC: 2013 Jul 18.
Published in final edited form as: Cell Stem Cell. 2012 Dec 20;12(1):88–100. doi: 10.1016/j.stem.2012.12.001

Figure 7. Genomic instability in p21-null cells can be restored by reduction of Sox2 levels.

Figure 7

(A) Lack of p21 leads to an increase in γH2AX staining, which is rescued by Sox2 knockdown in neurosphere cells (n = 3). (B) Immunostaining for GFAP (blue), γH2AX (green) and 53BP1 (red) in wild-type (WT), p21-null or p21-null/Sox2-het mice. White arrows indicate triple positive cells. (C) Immunostaining for GFAP (red) and Nestin (blue) and RPA (green) in wild-type (WT), p21-null or p21-null/Sox2-het mice. White arrows indicate triple positive cells. (D) Immunostaining for DCX (blue) and RPA (green) in wild-type (WT), p21-null or p21-null/Sox2-het mice. White arrows indicate DP cells. (E) Graph showing the proportions of γH2AX and GFAP DP cells that are also positive for 53BP1 in wild type (WT), p21-null or p21-null/Sox2-het mice (n = 3 animals per genotype). (F) Graph showing the proportions of Nestin and GFAP DP cells that are also positive for RPA (left bars) and of DCX-positive neuroblasts that are also RPA-positive in wild-type (WT), p21-null or p21-null/Sox2-het mice (n = 3). Data are represented as the average ± s.e.m. of the indicated number of the experiments (n) (*p<0.05; **p<0.01; ***p<0.001). Scale bars: in B and C, 10 μm; in D, 5 μm