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Open Access Research article

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

Junji Lin, Xu Wang and Richard I Dorsky*

Author Affiliations

Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, UT 84132, USA

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BMC Developmental Biology 2011, 11:73  doi:10.1186/1471-213X-11-73

Published: 2 December 2011



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.


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.


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.

Wnt; APC; Stat3; progenitor; zebrafish