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Fig. S5 eaf1 and eaf2 antagonize Wnt/β-catenin signaling. (A) The expression of axin2, a bona fide direct target of Wnt/β-catenin signaling at bud stage, was enhanced after knockdown of eaf1 (b,e) or eaf2 (c,f) (red arrows). (B) The offspring of apc+/- × apc+/- were genotyped by sequencing the mutant allele DNA fragment amplified from genomic DNA extracted from WISH-stained embryos. The embryos with normal opl expression contain the wild-type allele (C/C) (a,d), whereas the embryos with reduced opl expression contain the heterozygous allele (C/T) (b,e) and the embryos with strongly reduced opl expression contain the homozygous mutated allele (T/T) (c,f). (C) β-catenin1-MO, but not β-catenin2-MO, partially rescued the anterior brain defects in Eaf morphants. (D) At the 30% gastrula stage, β-catenin2- MO partially reduced the increased gsc expression associated with Eaf morphants (a-h); both β-catenin1-MO and β-catenin2-MO partially reduced the increased gsc expression of Eaf2-MO1 morphants at the sphere stage (i-m), and β-catenin2-MO was more effective (m). (A-C) Dorsal view, anterior to the left; (Da-g,i-l) dorsal view.