Fig. 3

Loss of p53 does not rescue sbds organogenesis defects. (A) The body curvature observed in Sbds^ATG MO-injected zebrafish embryos is attenuated in Sbds^ATG/p53^ATG MO-injected embryos at 48 hpf. (B) The p53 transcriptional targets Δ113p53 and p21 are induced upon injection of Sbds^ATG MO, as assessed by semi-quantitative PCR; co-injection of p53^ATG MO abrogates this response. Error bars indicate s.e.m. (C) The 72-hpf pancreatic progenitor phenotype induced by the Sbds^ATG MO is not rescued by co-injection of p53^ATG MO (arrows). (D) The absence of mpo-expressing neutrophils in the intermediate cell mass of Sbds^ATG/p53^ATG MO-injected embryos was detected at 24 hpf (arrowheads). (E) Co-injection of p53^Spl MO and Sbds^ATG MO into ptf1a:eGFP;ins:mCherry embryos does not rescue the defective expansion of pancreatic progenitor cells (arrows). (F) Genetic loss of p53 in p53^zdf1/zdf1 embryos does not rescue the Sbds^ATG MO-induced neutrophil phenotype, as assessed by in situ hybridization for mpo at 24 hpf (arrowheads). (G) The Sbds^ATG MO-induced pancreatic progenitor defect is not rescued in p53^zdf1/zdf1;ptf1a:eGFP;ins:mCherry embryos at 72 hpf.