Fig. 7

Fig. 7  Expression of pdx1, insulin, somatostatin (PPSS2), glucagon, ptf1a and trypsin in control (hsp70:Gal4 neg; UAS:N^ICDpos or hsp70:Gal4pos; UAS:N^ICDneg) and N^ICD-expressing (hsp70:Gal4pos; UAS:N^ICDpos) embryos heat shocked at different time points. Markers analyzed are indicated at the top of each subset of panels, while the time point of the first heat shock (HS) is indicated on the left. For each gene expression test, mono-genic control embryos (hsp70:Gal4 neg or UAS:N^ICDneg) are on the left and bi-genic embryos (hsp70:Gal4pos and UAS:N^ICDpos) are on the right. pdx1 (A–C); precursors, expressing pdx1, are increased in number when bi-genic embryos are heat shocked at 20 hpf or before (A′, B′, C′) indicating that Notch activation leads to proliferation of precursors. ins and sst (D–I); differentiation of insulin- and somatostatin-producing cells is completely blocked only when bi-genic embryos are heat shocked at 12 hpf (D′ and G′). glu (J–L); differentiation of glucagon-producing cells is completely blocked when bi-genic embryos are heat shocked at 20 hpf or before (J′ and K′) and severely impaired in embryos heat shocked at 30 hpf (L′). ptf1a and try (M–P); bigenic embryos heat shocked at 30 hpf fail to differentiate the exocrine pancreas (M′, N′, O′, P′). The stage at which the embryos were analyzed is indicated within each frame. Individual embryos were genotyped by PCR for presence or absence of each transgene. Embryos are in ventral views with anterior to the left.