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Fig. 8. Neural tissue development involves BMP/SMAD1-independent FGFR activity. (A-D) Stage 26 tailbud embryos immunostained for NCAM. (A) Untreated embryo; (B) class V embryo treated from stage 7 to 26 with 120 μM SU5402; (C) embryo treated similarly with SU5402 and which had received injection at the four-cell stage of lacZ, tBR (400 pg), noggin (250 pg) and Smad6 (4 ng) RNAs; (D) embryo treated similarly with SU5402 and injected at blastula stage 9 with 1 ng Noggin protein. BMP inhibitors converted epidermis into cement gland (cement glands are outlined in B-D), but did not rescue neural tissue in class V embryos. (E-G) These embryos received the same treatment and injection as in A-C, but were harvested at the early gastrula stage 10.5, and analysed for Sox2 expression. No rescue of Sox2 expression was obtained upon injection of the triple inhibitor combination in class V embryos. (H) Eight-cell embryos were injected in all four animal blastomeres with Smad6 RNA (1 ng/blastomere) and cultured in absence or in presence of 120 μM SU5402 from stage 7, as indicated. Animal caps were excised at blastula stage 9, further cultured in the inhibitor until late gastrula stage 13, and harvested at tailbud stage. Siblings were class V in this experiment. Neural induction by Smad6 is suppressed in absence of FGFR activity. |
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ncam1 (neural cell adhesion molecule 1) gene expression in Xenopus laevis embryo, assayed via in situ hybridization, NF stage 26, lateral view, anterior left, dorsal up |
