Fig. 7. Perturbation of the oral/aboral axis and the consequences for LvTbx2/3 expression. (A,B) Control embryos depicting normal expression of EctoV and LvBrac. (A) Cross-sectional view of EctoV oral ectoderm distribution in the late gastrula. (B) Mid-gastrula surface view of normal blastopore and somodael LvBrac expression. (C,D) Injection of LvG-cadherin mRNA animalizes the embryo by binding to endogenous ß-catenin and preventing its nuclear localization. These embryos lack endoderm and mesoderm and, as previously reported, express the EctoV antigen uniformly (C). They do not express aboral LvTbx2/3 (D). (E,F) NiCl₂ ventralization. (E) LvBrac expression expands to all ectoderm cells after ventralization with NiCl₂. (F) LvTbx2/3 is not expressed in any germ layer of these embryos. (G,H) Ectopic expression of BMP2/4 radializes the ectoderm of the embryo, as indicated by the formation of multiple triradiate spicules (Angerer et al., 2000). Such embryos express normal levels of vegetal LvBrac around the blastopore but do not express oral LvBrac (G) and aboral LvTbx2/3 in the tissue of any germ layer (H), indicating that ectopic expression of BMP2/4 antagonizes normal specification events along the A/V axis and in the O/A axis in all germ layers. (I,J) Disruption of the extracellular matrix with ßAPN, a drug that prevents collagen crosslinking, results in the failure to express oral LvBrac, but vegetal expression of LvBrac is, apparently, unaffected (I). (J) ßAPN also prevents LvTbx2/3 expression.