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Fig. 1 SNX17 regulates Notch signaling in zebrafish. (A) Expression pattern of SNX17 at day 2 as detected by in situ hybridization. SNX17 was enriched in the liver and pancreas (arrows) at this stage. (B) Efficiencies of splice-blocking MOs in inducing the alternative splicing of SNX17 mRNA as determined by RT-PCR. (C) Knockdown of SNX17 did not disrupt liver development. lfabp is a marker for hepatocytes. (D, E) The expression of the endocrine β-cell marker insulin (ins) was mildly increased while the exocrine marker trypsin (trp) was down-regulated in SNX17 morphants. The trp defect was rescued by co-injection of mRNA encoding human SNX17. (F) Knockdown of SNX17 or mib enhanced the expression of pro-neuronal marker huC. Injection of mRNA encoding the NICD rescued the SNX17-knockdown induced neurogenic defect. (G) Real-time RT-PCR analysis of huC and her/hes family endogenous Notch target genes. β-actin is the reference and data represent mean ± SD from three independent assays.