Skip to main content
. 2014 Dec 9;9:27. doi: 10.1186/1749-8104-9-27

Figure 4.

Figure 4

Expression of an activated mutant form of Ctnnb1 in the neural retina (NR) induces ciliary epithelium (CE)- like cell fate transformation. Transverse sections of mutant eyes induced with tamoxifen to express Ctnnb1 lox(ex3) in Sox2-expressing cells at E11.5 were analyzed at E15.5. (A-I) In situ hybridization for Bmp4 (A, D) and Msx1 (B, E) shows specific expression of these CE genes in ectopic regions, which accumulate β-Catenin in serial sections (G). Loss of NR fate is evident through in situ hybridization for Otx2 (F) normally marking the NR (C). Yellow and white arrowheads indicate two regions of β-Catenin accumulation across the different markers in serial sections (D-I). The cell fate transformation is accompanied by loss of proliferative capacity as seen by anti-Ki67 immunofluorescence (H) and loss of SOX2 (I). (J-O) Double immunofluorescence for β-Catenin and Ki67 (J-L) and β-Catenin together with SOX2 (M-O) reveal that areas of β-Catenin accumulation in induced Sox2 CreERT2/+;Ctnnb1 lox(ex3)/+ retinas are accompanied by the loss of proliferative capacity and the specific reduction of SOX2 indicating loss of NR fate. Two representative regions of β-Catenin accumulation are indicated across the three markers with yellow arrows (panels J- O). Scale bars: 200 μm.