PUBLICATION

Sonic hedgehog is required early in pancreatic islet development

Authors
diIorio, P.J., Moss, J.B., Sbrogna, J.L., Karlstrom, R.O., and Moss, L.G.
ID
ZDB-PUB-020402-4
Date
2002
Source
Developmental Biology   244(1): 75-84 (Journal)
Registered Authors
diIorio, Philip, Karlstrom, Rolf, Moss, Jennifer Barnett, Moss, Larry Gene, Sbrogna, Jen
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Embryonic Induction
  • Gastrula/drug effects
  • Gastrula/physiology*
  • Gene Expression Regulation, Developmental*
  • Green Fluorescent Proteins
  • Hedgehog Proteins
  • In Situ Hybridization
  • Islets of Langerhans/embryology*
  • Luminescent Proteins/genetics
  • Mutation
  • Pancreas/embryology
  • Signal Transduction/drug effects
  • Signal Transduction/genetics
  • Trans-Activators/genetics*
  • Veratrum Alkaloids/pharmacology
  • Zebrafish/embryology*
PubMed
11900460 Full text @ Dev. Biol.
Abstract
Pancreatic organogenesis relies on a complex interplay of cell-autonomous and extracellular signals. We demonstrate that the morphogen sonic hedgehog (Shh) is required for pancreatic development in zebrafish. Genetic mutants of Shh and its signaling pathway establish this dependence as specific to endocrine, but not exocrine, pancreas. Using cyclopamine to inhibit hedgehog signaling, we show that transient Shh signaling is necessary during gastrulation for subsequent differentiation of endoderm into islet tissue. A second hedgehog-dependent activity occurring later in development was also identified and may be analogous to the known action of Shh in gut endoderm to direct localization of pancreatic development. The early action of Shh may be part of a more general process allowing neuroendocrine cells to originate in nonneuroectodermally derived tissues.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping