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. 2011 Feb 1;138(3):443–454. doi: 10.1242/dev.055178

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Fig. 8. — Pax6-haploinsufficiency significantly rescues the Sox2-mutant NR. (A,B,J,K,S,T) Comparison of SOX2 immunohistochemistry (red) with αP0^CREiresGFP expression (green) in Pax6 single mutant (Sox2^cond/+; αP0^CREiresGFP; Pax6^Sey/+), Sox2 Pax6 double mutant (Sox2^cond/cond; αP0^CREiresGFP; Pax6^Sey/+) and Sox2 single mutant (Sox2^cond/cond; αP0^CREiresGFP) eyes indicating little to no SOX2 expression in the Sox2 single mutant compared with the other two genotypes. (C,L,U) β-gal activity illustrating the progeny of all αP0^CREiresGFP-expressing cells indicates rescue of αP0^CREiresGFP expression in Sox2 Pax6 double mutants. (D,M,V) β-tubulin III (red) shows maintenance of neuronal differentiation capacity in Pax6 single mutants and Sox2 Pax6 double mutants but not in Sox2 single mutants. (E-I,N-R,W-AA) In situ hybridization of Notch1 (E,N,W), Hes5 (F,O,X), NeuroD1 (G,P,Y), Rax (H,Q,Z) and Chx10 (I,R,AA) shows maintenance of prospective NR markers in the Sox2 Pax6 double mutants. Scale bar: 200 μm.