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SEL1L deficiency impairs growth and differentiation of pancreatic epithelial cells

Shuai Li1, Adam B Francisco, Robert J Munroe

  • 1Department of Animal Science, College of Agriculture and Life Sciences, Cornell University, Ithaca, NY 14850, USA.

BMC Developmental Biology
|February 23, 2010
PubMed
Abstract

Insights

Suppressor enhancer lin-12/Notch 1 like (Sel1l) is crucial for pancreatic development. Loss of Sel1l in mice impairs pancreatic cell differentiation and growth, highlighting its role in embryonic organogenesis.

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • The vertebrate pancreas develops from multipotent progenitors.
  • Understanding pancreatic organogenesis is key for diabetes mellitus cell therapies.
  • The role of Suppressor enhancer lin-12/Notch 1 like (Sel1l) in pancreatic development is unknown.

Purpose of the Study:

  • To investigate the function of Sel1l during mouse pancreatic development.
  • To characterize the pancreatic phenotype of Sel1l-deficient mice.

Main Methods:

  • Gene trap mutation in Sel1l.
  • Phenotypic analysis of Sel1l mutant mouse embryos.
  • Pharmacological inhibition of Notch signaling.

Main Results:

  • Sel1l is expressed during pancreatic endocrine and exocrine lineage differentiation.
  • Sel1l homozygous mutant mice exhibit prenatal lethality.
  • Mutant embryos show impaired pancreatic epithelial morphology and cell differentiation, with cells arrested in the progenitor state.
  • Notch signaling inhibition partially rescues the Sel1l mutant phenotype.

Conclusions:

  • Sel1l is essential for the growth and differentiation of pancreatic epithelial cells.
  • Sel1l plays a critical role in mouse embryonic pancreatic development.

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