Fig. 2. inscuteable expression is dependent on the Snail family of proteins. (A,C,E,G) Stage 9 embryos. (B,D,F,H) Stage 10 embryos. All embryos are ventral views. RNA in situ hybridization reveals the mRNA expression of inscuteable is significantly lower in osp29 mutant (C,D) than in wild-type embryos (A,B). Note that some localized mRNA is still present in osp29 embryos. (E-H) Loss of inscuteable expression can be efficiently rescued in embryos expressing transgenic Snail family of proteins. (E,F) Embryos with P[snail] transgene; (G,H) embryos with P[wor, esg] transgenes. The P[wor, esg] was generated by recombination of the two individual transgenes (Ashraf et al., 1999), with each under the control of 2.8 kb snail promoter, including the neuroblast expression element (Ip et al., 1992; Ip et al., 1994). For this and following figures, some of the mutant embryos shown have morphological defects that are due to the requirement of Snail in gastrulation. The morphological phenotype is used whenever possible to identify embryos that harbor the mutation. The gastrulation phenotype has no direct consequence on the expression of CNS markers. This is based on the observations that rescue of morphological defect by snail driven by mesoderm promoter alone cannot rescue the CNS defect, and worniu and escargot transgenes can rescue CNS defect but not gastrulation defect (e.g. see G,H).
