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Intra-endodermal interactions are required for pancreatic beta cell induction.

Won-Suk Chung¹, Didier Y R Stainier

¹Department of Biochemistry and Biophysics, and the Diabetes Center, University of California, San Francisco, 1550 4th Street, San Francisco, CA 94158, USA.

Developmental Cell

|April 16, 2008

Summary

This summary is machine-generated.

Pancreatic beta cell development relies on Hedgehog/Smoothened signals from neighboring cells during early development, not the beta cells themselves. This clarifies signaling roles in pancreas formation.

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Area of Science:

Developmental Biology
Endocrinology
Molecular Signaling

Background:

The precise cellular origins of signals regulating pancreatic beta cell induction remain unclear.
Hedgehog/Smoothened signaling exhibits a dual role, promoting beta cell development in zebrafish gastrulation but inhibiting it later in amniotes.

Purpose of the Study:

To elucidate the cellular source of signals governing pancreatic beta cell induction.
To resolve the paradoxical roles of Hedgehog/Smoothened signaling in pancreas development across species.

Main Methods:

Utilized cell transplantation experiments in zebrafish embryos.
Analyzed the spatial and temporal requirements of Smoothened function during endoderm development.

Main Results:

Smoothened function is not cell-autonomous in beta cell precursors.
Requirement for Smoothened signaling resides in lateral endodermal neighbors of beta cell precursors.
These lateral neighbors give rise to the exocrine pancreas and intestine.

Conclusions:

Pancreatic beta cell induction requires cell-nonautonomous Smoothened function during gastrulation.
This signaling facilitates crucial intra-endodermal interactions for beta cell specification.
Identified an unexpected cellular source regulating beta cell specification and complex endodermal patterning.