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Fig. 6
Fgf signaling negatively regulates hepatic competence. (A-H) Enhancing Fgf signaling by overexpressing caFgfr1 via heat-shock at 26 (A-D) or 30 (E-H) hpf greatly reduced or abolished the effect of Wnt8a overexpression on ectopic hepatocyte formation, whereas it did not block its effect on the increase of liver size in wnt2bb mutants. Fewer ectopic hepatocytes appeared to be induced in embryos that overexpressed both Wnt8a and caFgfr1 than in ones that overexpressed Wnt8a only (a representative comparison is shown in D versus C and H versus G, brackets, n=6 out of 6), but liver size was comparable between these embryos. (I-L) Reducing Fgf signaling with the Fgfr inhibitor SU5402 greatly enhanced the effect of Wnt8a overexpression on ectopic hepatocyte formation. Embryos that overexpressed Wnt8a from a 30 hpf heat-shock exhibited significantly more ectopic hepatocytes when treated with SU5402 from 24 to 38 hpf [L (n=6 out of 6) versus K (n=5 out of 5), brackets]. SU5402 treatment in the absence of Wnt8a overexpression did not induce ectopic hepatocytes, but increased liver size and reduced pancreatic size (J, n=5 out of 5). Ventral views, anterior up. Scale bars: 50 μm.