PUBLICATION

The development of zebrafish pancreas affected by deficiency of Hedgehog signaling

Authors
Korzh, S., Winata, C.L., Gong, Z., Korzh, V.
ID
ZDB-PUB-210605-13
Date
2021
Source
Gene expression patterns : GEP   41: 119185 (Journal)
Registered Authors
Gong, Zhiyuan, Korzh, Svitlana, Korzh, Vladimir, Winata, Cecilia Lanny
Keywords
annular pancreas, elastase, green fluorescent protein (GFP), pancreas, transgenic, zebrafish
MeSH Terms
  • Animals
  • Hedgehog Proteins*/genetics
  • Pancreas
  • Signal Transduction*
  • Smoothened Receptor/genetics
  • Smoothened Receptor/metabolism*
  • Zebrafish*/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
34087472 Full text @ Gene Expr. Patterns
Abstract
The pancreas development depends on complex regulation of several signaling pathways, including the Hedgehog (Hh) signaling via a receptor complex component, Smoothened, which deficiency blocks the Hh signaling. Such a defect in birds and mammals results in an annular pancreas. We showed that in developing zebrafish, the mutation of Smoothened or inhibition of Hh signaling by its antagonist cyclopamine caused developmental defects of internal organs, liver, pancreas, and gut. In particular, the pancreatic primordium was duplicated. The two exocrine pancreatic primordia surround the gut. This phenomenon correlates with a significant reduction of the gut's diameter, causing the annular pancreas phenotype.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping