ZFIN ID: ZDB-PUB-111206-1
Progenitor expansion in apc mutants is mediated by Jak/Stat signaling
Lin, J., Wang, X., and Dorsky, R.I.
Date: 2011
Source: BMC Developmental Biology   11(1): 73 (Journal)
Registered Authors: Dorsky, Richard, Lin, Junji, Wang, Xu
Keywords: none
MeSH Terms:
  • Adenomatous Polyposis Coli Protein/genetics*
  • Adenomatous Polyposis Coli Protein/metabolism
  • Animals
  • Base Sequence
  • Embryo, Nonmammalian/metabolism
  • Janus Kinases/genetics
  • Janus Kinases/metabolism*
  • Molecular Sequence Data
  • Neural Stem Cells/cytology
  • Neural Stem Cells/metabolism
  • STAT3 Transcription Factor/metabolism*
  • Signal Transduction*
  • Stem Cells/cytology*
  • Stem Cells/metabolism
  • Transcriptional Activation
  • Wnt Signaling Pathway/genetics
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
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.