Stabilization of β-catenin impacts pancreas growth

Patrick W. Heiser, Janet Lau, Makoto M. Taketo, Pedro L. Herrera, Matthias Hebrok

Research output: Contribution to journalArticlepeer-review

200 Scopus citations

Abstract

A recent study has shown that deletion of β-catenin within the pancreatic epithelium results in a loss of pancreas mass. Here, we show that ectopic stabilization of β-catenin within mouse pancreatic epithelium can have divergent effects on both organ formation and growth. Robust stabilization of β-catenin during early organogenesis drives changes in hedgehog and Fgf10 signaling and induces a loss of Pdx1 expression in early pancreatic progenitor cells. Together, these perturbations in early pancreatic specification culminate in a severe reduction of pancreas mass and postnatal lethality. By contrast, inducing the stabilized form of β-catenin at a later time point in pancreas development causes enhanced proliferation that results in a dramatic increase in pancreas organ size. Taken together, these data suggest a previously unappreciated temporal/spatial role for β-catenin signaling in the regulation of pancreas organ growth.

Original languageEnglish
Pages (from-to)2023-2032
Number of pages10
JournalDevelopment (Cambridge)
Volume133
Issue number10
DOIs
StatePublished - May 2006
Externally publishedYes

Keywords

  • FGF
  • Hedgehog
  • Mouse
  • Organ size
  • Pancreas development
  • Pancreatomegaly
  • Pdx1
  • Wnt
  • β-catenin

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