Fig. 7. Inhibition of Ral signalling in prospective mesoderm causes gastrulation defects. Effect of XralB S28N on early development. Embryos were co-injected in each blastomere of 4-cell stage embryos with XralB S28N (500 pg/blastomere), and ß-Galactosidase (500 pg/blastomere) RNAs, in the animal apical hemisphere (A), in the marginal zone (B) or in the bottom of the vegetal hemisphere (C). (D) Effect of the Ral binding domain of RLIP on early development. Embryos at the 4-cell stage were injected in the marginal zone with 500 pg/blastomere of mRNA encoding the Ral binding domain of RLIP (RalBD). These embryos remained blocked during gastrulation, even when control embryos had reached stage 22. (E) Embryos injected in the marginal zone with mRNA encoding wild-type XralB (4x 750 pg). The site of RNA expression was monitored by detection of co-injected ß-galactosidase expression. (2) and (4) show embryos corresponding to sibling controls at stage 17. Embryos had X-gal-stained cells in the marginal zone. Arrows in Band D indicate the ring corresponding to the open blastopore. (F) Rescue of XralB S28N by coexpression with wild-type XralB. All embryos were microinjected in marginal zone at 4-cell stage with XralB S28N (4x 750 pg) mRNA or co-injected with wild-type XralB (4x 1.5 ng) mRNA. Vegetal view of embryos all at the same time after injection. (G) Protein expressed in embryos injected with XralB S28N and wild-type XralB mRNAs were controlled by western blot.

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