Fig. 3. Effects of RALDH1 and RALDH3 inactivation, alone or in combination, on the RA-dependent activity of a reporter transgene. Distribution of ß-galactosidase activity driven by the RARE-lacZ transgene in wild-type (A,E,I), Aldh1a1-null (B,F,J), Aldh1a3-null (C,G,K) and Aldh1a1/3-null (D,H,L) mutants at E10.5 (A-D), E11.5 (E-H) and E13.5 (I-L). Red arrowheads (E,H) indicate dorsal and ventral eyelid grooves. Black arrowhead (J) indicates the most peripheral portion of the dorsal retina where RARE-lacZ activity is not abolished in Aldh1a1-null fetuses. The faint staining observed at E10.5 in the retina of Aldh1a1/3-null mutants (D) reflects a residual activity of the ß-galactosidase synthesized at an earlier stage, as no lacZ mRNA can be detected using in situ hybridization. Note also that the ß-galactosidase activity detected at E13.5 in the ventral retina of the Aldh1a3-null fetus (K) results from expression of Aldh1a1. c, presumptive corneal ectoderm; d, dorsal retina; le, lens; m, periocular mesenchyme; o, optic nerve; rpe, retinal pigment epithelium; v, ventral retina. Scale bar in L: 40 µm for A-C; 50 µm for D-F; 80 µm for G-I.