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. 2019 Dec 16;146(24):dev168799. doi: 10.1242/dev.168799

Fig. 3.

Fig. 3.

Wnt16-Fzl1/2/7 signaling antagonizes the Wnt1/Wnt8-Fzl5/8-JNK pathway during the ANE restriction mechanism. (A) The expression of the ANE marker foxq2 expanded in embryos overexpressing wnt16 mRNA at the mesenchyme blastula stage (compare Ab,d with Ab,c). (B) At mesenchyme blastula stage, the expression of the cardinal regulator foxq2 was expanded in ΔFzl5/8 mRNA-injected embryos (Bc) compared with control embryos (Ba). In the absence of Wnt16, foxq2 expression was severely downregulated in ANE (Bb), whereas Wnt16 morphants co-injected with ΔFzl5/8 rescued the expression of ANE factors, showing a normal or expanded foxq2 expression (91%) (Bd). (C) Control embryos showing foxq2 expression at the 120-cell and mesenchyme blastula stage (24 hpf) (Ca,Ce). ANE expression of foxq2 was completely eliminated in Fzl1/2/7 morpholino-injected embryos (Cb,Cf). At the 120-cell stage, foxq2 was expressed in embryos injected with wnt16 mRNA (Cc). At mesenchyme blastula stage, foxq2 expression was strongly upregulated and expanded towards the posterior pole in embryos injected with wnt16 mRNA (Cg). Overexpression of wnt16 in a Fzl1/2/7 morphant background produced a completely elimination of foxq2 expression, mimicking the Fzl1/2/7 knockdown phenotype (Cd,Ch). MO, morpholino; ΔFzl5/8, dominant negative Fzl5/8. Scale bars: 20 µm.