The pes mutant phenocopies SbdsATG MO-induced p53-independent defects in pancreas development. (A) In situ hybridization at 24 hpf demonstrates pes expression in the eye and central nervous system. At 72 hpf, pes expression is detected in endoderm, including the developing pancreas. (B) The peshi2Tg/hi2Tg phenotype includes axis defects (tail curvature), a small dark head and a small eye. (C) Semi-quantitative RT-PCR of peshi2Tg/hi2Tg embryos reveals activation of the p53 target genes Δ113p53 (24-fold, P<0.0001) and p21 (2.4-fold, P<0.01). Error bars indicate s.e.m. (D) Loss of p53 does not rescue axis defects in peshi2Tg/hi2Tg embryos. Representative images of siblings (sib) generated either from a peshi2Tg/WT incross and injected with or without (Mock) p53ATG MO or p53Spl MO, or from a peshi2Tg/WT;p53zdf1/zdf1 incross. Asterisks indicate siblings displaying the pes phenotype. See supplementary material Fig. S6 for quantification. (E) peshi2Tg/hi2Tg embryos exhibit a p53-independent defect in expansion of ptf1-expressing pancreatic progenitor cells. The pancreatic progenitor defect in 72-hpf peshi2Tg/hi2Tg;ptf1a:eGFP;ins:mCherry embryos is not rescued by p53 MO-mediated knockdown, nor by genetic inactivation of p53 as assessed by incross of peshi2Tg/WT;p53zdf1/zdf1;ptf1a:eGFP;ins:mCherry fish.