Fig. 2

Fig. 2 β-catenin levels mediate differential liver phenotypes in APC mutant zebrafish. (A–D) IHC for β-catenin at 72 hpf (40x, close-up as inset) revealed an increase in both cytoplasmic (APC^+/-: 39.4 ± 13.4% (% of hepatocytes with cytoplasmic β-catenin ± SD) vs. 9.8 ± 3.8%; n = 5, p = 0.0006) and nuclear staining (20.8 ± 8.2% vs. 4.3 ± 1.8%; n = 5, p = 0.0012) in the hepatocytes of APC^+/- embryos compared to wild-type. While liver-specific IHC could not be performed in the APC^-/-embryos, β-catenin staining was widely positive in the region of the endoderm. (E–I) MO (40 μM) injected in the progeny of an APC^+/- incross at the one-cell stage revealed a shift in liver phenotype distribution. (E) A graphical depiction of the shift in distribution of liver phenotypes with correlated genotypes in β-catenin MO injected embryos compared to controls. Distribution of control MO phenotypes (genotype): 59/234 normal (92% APC^+/+, 8% APC^+/-), 114/234 big (APC^+/-), 61/234 absent (APC^-/-); β-catenin MO phenotypes: 156/211 normal (40% APC^+/+, 60% APC^+/-), 32/211 big (APC^+/-), 13/211 absent and 10/211 rescue (APC^-/-). (F–I) Representative lfabp in situ hybridization phenotypes observed in β-catenin MO injected embryos at 72 hpf.