PUBLICATION

Different levels of Notch signaling regulate quiescence, renewal and differentiation in pancreatic endocrine progenitors

Authors
Ninov, N., Borius, M., and Stainier, D.Y.
ID
ZDB-PUB-120412-11
Date
2012
Source
Development (Cambridge, England)   139(9): 1557-1567 (Journal)
Registered Authors
Ninov, Nikolay, Stainier, Didier
Keywords
notch, endocrine, pancreas, progenitor, transgenic, zebrafish
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Cell Differentiation/physiology*
  • Cell Proliferation
  • Fluorescent Antibody Technique
  • Islets of Langerhans/cytology*
  • Larva/metabolism
  • Larva/physiology
  • Receptors, Notch/metabolism*
  • Signal Transduction/physiology*
  • Stem Cells/physiology*
  • Zebrafish/growth & development*
  • Zebrafish/metabolism
PubMed
22492351 Full text @ Development
Abstract

Genetic studies have implicated Notch signaling in the maintenance of pancreatic progenitors. However, how Notch signaling regulates the quiescent, proliferative or differentiation behaviors of pancreatic progenitors at the single-cell level remains unclear. Here, using single-cell genetic analyses and a new transgenic system that allows dynamic assessment of Notch signaling, we address how discrete levels of Notch signaling regulate the behavior of endocrine progenitors in the zebrafish intrapancreatic duct. We find that these progenitors experience different levels of Notch signaling, which in turn regulate distinct cellular outcomes. High levels of Notch signaling induce quiescence, whereas lower levels promote progenitor amplification. The sustained downregulation of Notch signaling triggers a multistep process that includes cell cycle entry and progenitor amplification prior to endocrine differentiation. Importantly, progenitor amplification and differentiation can be uncoupled by modulating the duration and/or extent of Notch signaling downregulation, indicating that these processes are triggered by distinct levels of Notch signaling. These data show that different levels of Notch signaling drive distinct behaviors in a progenitor population.

Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping