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Background  Mutations in  APC , a negative regulator of the Wnt/ß-catenin pathway, can cause cancer as well as profound developmental defects. In both cases, affected cells adopt a proliferative progenitor state and fail to differentiate. While the upregulation of some target genes of Wnt/ß-catenin signaling has been shown to mediate these phenotypes in individual tissues, it is unclear whether a common mechanism underlies the defects in  APC  mutants.    Results  Here we show that  stat3 , a known oncogene and a target of ß-catenin in multiple tissues, is upregulated in  apc  mutant zebrafish embryos. We further demonstrate that Jak/Stat signaling is necessary for the increased level of proliferation and neural progenitor gene expression observed in  apc  mutants.    Conclusions  Together, our data suggest that the regulation of Jak/Stat signaling may represent a conserved mechanism explaining the expansion of undifferentiated cells downstream of  APC  mutations.

Progenitor expansion in apc mutants is mediated by Jak/Stat signaling