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Fig. 5. Absence of RA signaling in the periocular mesenchyme results in severe ocular defects. (A-E) External views of the ocular region of E14.5 fetuses (genotypes as indicated). (F-L) Frontal histological sections through heads of E14.5 (F-J) and E18.5 (K,L) fetuses. (M,N) Distribution of ß-galactosidase activity driven by the R26R transgene in E10.5 embryos bearing the Wnt1-Cre transgene either in a wild-type genetic background (M, WT^{NCC+/+ lacZ}), or in a genetic background containing loxP-flanked Rarb and Rarg genes (N, Rarb/g^{NCC–/– lacZ}). In both WT^{NCC+/+ lacZ} and Rarb/g^{NCC–/– lacZ} embryos, the ß-galactosidase staining is identical, indicating that ablation of RARß and RAR does not alter the migration of neural crest cells (NCCs) in the periocular mesenchyme. Asterisks (I,J,L) indicate undifferentiated mesenchyme replacing the eyelids and cornea; dotted lines (F-J) indicate the equatorial plane of the lens; arrowhead (L) points to the coloboma of the retina. a, anterior chamber; c, cornea; d, dorsal retina; e, eyelid; i, iris; j, conjunctival sac; le, lens; m, periocular mesenchyme; o, optic nerve; rpe, retinal pigment epithelium; r, retrolenticular membrane; s, sclera; v, ventral retina. Scale bar in N: 120 µm for F-J; 250 µm for K,L; 25 µm for M,N.

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