|ZFIN ID: ZDB-PUB-111206-1|
|Source:||BMC Developmental Biology 11(1): 73 (Journal)|
|Registered Authors:||Dorsky, Richard, Lin, Junji, Wang, Xu|
|PubMed:||22136118 Full text @ BMC Dev. Biol.|
Mutations in APC, a negative regulator of the Wnt/beta-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/beta-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 beta-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.