Fig. 4. Gli3 is not required to establish DV gene expression domains or to inhibit activating Shh signaling. (A-I) RNA in situ hybridization for Pax7 (A-C, dorsal marker) and Gli1 (D-F, ventral marker) and immunohistochemistry for Nkx6.1 (G-I, ventral marker) on transverse sections of E10.5 mouse embryos show that expression of these genes in Gli3^-/- and En1-Gli3 cko mutants is comparable to WT. (J-M) H+E staining on P0 (J) and E12.5 (K-M) sagittal sections. The phenotypes of the Sc, Ic and Is are comparable in P0 En1-Gli3;Smo cko and En1-Gli3 cko mutants. Note that the Cb is small and unfoliated, with a thin external granule cell layer. (K-M) At E12.5, the size of r1 is increased in both En1-Gli3 and En1-Gli3;Smo cko mutants as compared with WT. v, ventral; d, dorsal. Scale bars: 125 µm in A-I; 500 µm in J; 200 µm in K-M.