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Fig. 3. Notch signalling is required for cell movements during proventriculus morphogenesis. Anti-Fkh(red)/anti-Dve (green) immunostaining of Dl (A-C), Notch (D-F), fng (G-I) and Su(H) (J-L) loss-of-function mutants at stage 12 (A,D,G,J), stage 15 (B,E,H,K) and stage 17 (C,F,I,L) of proventriculus development. Specification of the early proventriculus primordium is not affected in any of the mutants (compare with wild type, Fig. 1A), whereas cell movements leading to the keyhole structure at stage 15 (compare with wild type, Fig. 1C) and to the cardia structure at stage 17 (compare with wild type, Fig. 1D) do not take place, leading to block of invagination in mutants of the Notch signalling cassette. (M) Ectopic 14-3fkh-Gal4 mediated expression of the Notch ligand Dl causes a Notch-like phenotype, i.e. loss of invagination of ectodermal cells, as shown by anti-Dl (red)/anti-Dve (green) double staining. (N) Ectopic hsGal4 mediated expression of the Notch extracellular domain (N^ECD) also abrogates infolding of ectodermal cells at late stages of proventriculus development, visualised by anti-Dl(red)/anti-Dve(green) double staining. (O) Anti-Fkh (red)/anti-Dve (green) double staining showing that ectopic activation of the Notch signalling pathway causes ectopic cell movements (arrow). However, we do not observe changes in endodermal or ectodermal cell fate in these embryos.

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