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Progenitor expansion inapcmutants is mediated by Jak/Stat signaling

✍ Scribed by Junji Lin; Xu Wang; Richard I Dorsky

Publisher
BioMed Central
Year
2011
Tongue
English
Weight
642 KB
Volume
11
Category
Article
ISSN
1471-213X

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✦ Synopsis

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.

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