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Development ePress online publication date 12 Apr 2006
doi: 10.1242/dev.02366

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Research Article: Development and Disease

Stabilization of {beta}-catenin impacts pancreas growth


Patrick W. Heiser, Janet Lau, Makoto M. Taketo, Pedro L. Herrera, and Matthias Hebrok*
* Author for correspondence (e-mail: mhebrok{at}diabetes.ucsf.edu)

A recent study has shown that deletion of {beta}-catenin within the pancreatic epithelium results in a loss of pancreas mass. Here, we show that ectopic stabilization of {beta}-catenin within mouse pancreatic epithelium can have divergent effects on both organ formation and growth. Robust stabilization of {beta}-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 {beta}-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 {beta}-catenin signaling in the regulation of pancreas organ growth.


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