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Fig. 6b. FoxB1 suppresses anterior development via the expression of Wnt and FGF ligands. (L′) FoxB1 expands the expression domain of Wnt and FGF ligand genes in embryos. Together with β-gal mRNA, GR-FoxB1 mRNA (500 pg) was injected unilaterally into both dorsal and ventral animal blastomeres of 8-cell stage embryos. The expression of XWnt-8 (L′; st. 15/16), eFGF (M; st. 15/16), FGF3 (N and N′; st. 12.5) or FGF8 (O and O′; st. 12.5) analyzed by in situ hybridization is shown in purple and β-gal is stained in red. Upon overexpression of FoxB1, the expression of XWnt-8 expands laterally and ventrally around the posterior part of the embryo (arrowheads, L and L′). The expression of FGF ligands was also found to be expanded (arrowheads, M′). The injected side of the embryo is indicated by brackets. L, M, N, and O: posterior views with dorsal to the top; N′ and O′: dorsal view of (N) and (O), respectively, with anterior to the top; L′: lateral view of (L) with anterior to the left; L′: lateral view of (L) with anterior to the right. (P) FoxB1 requires the function of XWnt-8 and FGF ligands for suppression of anterior structures. GR-FoxB1 mRNA (500 pg) in combination with the indicated MOs (40 ng total per embryo) were injected into four animal blastomeres of 4-cell stage embryos. Suppression of the cement glands in FoxB1-overexpressing embryos was rescued efficiently by XWnt-8 MO. In contrast, the efficiency of eFGF MO was significantly less than that of XWnt-8 MO, and FGF3 MO showed a limited effect. (V) Summary of phenotypes shown in (P)U). (W) Summary of defects in the expression of retinal marker Rx2A. XWnt-8 MO reverses the defects in Rx2A expression caused by FoxB1 overexpression. While neither FGF3 MO nor a combination of all three MOs shows significant effects, eFGF MO has a weak rescue activity. |
