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

Developmental cell | Apr 15, 2008

The cellular origin of signals that regulate pancreatic beta cell induction is not clearly defined. Here, we investigate the seeming paradox that Hedgehog/Smoothened signaling functions during gastrulation to promote pancreatic beta cell development in zebrafish, yet has an inhibitory role during later stages of pancreas development in amniotes. Our cell transplantation experiments reveal that in zebrafish, Smoothened function is not required in beta cell precursors. At early somitogenesis stages, when the zebrafish endoderm first forms a sheet, pancreatic beta cell precursors lie closest to the midline; however, the requirement for Smoothened lies in their lateral neighbors, which ultimately give rise to the exocrine pancreas and intestine. Thus, pancreatic beta cell induction requires Smoothened function cell-nonautonomously during gastrulation, to allow subsequent intra-endodermal interactions. These results clarify the function of Hedgehog signaling in pancreas development, identify an unexpected cellular source of factors that regulate beta cell specification, and uncover complex patterning and signaling interactions within the endoderm.

Pubmed ID: 18410733 RIS Download

Mesh terms: Animals | Animals, Genetically Modified | Cell Differentiation | Cell Lineage | Cell Transplantation | Embryonic Induction | Endoderm | Hedgehog Proteins | Insulin-Secreting Cells | Mesoderm | Receptors, G-Protein-Coupled | Recombinant Fusion Proteins | Signal Transduction | Smoothened Receptor | Transgenes | Zebrafish | Zebrafish Proteins

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Associated grants

  • Agency: NIDDK NIH HHS, Id: R01 DK075032-02
  • Agency: NIDDK NIH HHS, Id: U19 DK061245
  • Agency: NIDDK NIH HHS, Id: R01 DK075032
  • Agency: NIDDK NIH HHS, Id: R01 DK075032-01A1
  • Agency: NIDDK NIH HHS, Id: DK75032
  • Agency: NIDDK NIH HHS, Id: DK61245

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