Email updates

Keep up to date with the latest news and content from BMC Developmental Biology and BioMed Central.

Open Access Research article

SEL1L deficiency impairs growth and differentiation of pancreatic epithelial cells

Shuai Li1, Adam B Francisco1, Robert J Munroe2, John C Schimenti2 and Qiaoming Long1*

Author Affiliations

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

2 Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14850, USA

For all author emails, please log on.

BMC Developmental Biology 2010, 10:19  doi:10.1186/1471-213X-10-19

Published: 19 February 2010



The vertebrate pancreas contains islet, acinar and ductal cells. These cells derive from a transient pool of multipotent pancreatic progenitors during embryonic development. Insight into the genetic determinants regulating pancreatic organogenesis will help the development of cell-based therapies for the treatment of diabetes mellitus. Suppressor enhancer lin12/Notch 1 like (Sel1l) encodes a cytoplasmic protein that is highly expressed in the developing mouse pancreas. However, the morphological and molecular events regulated by Sel1l remain elusive.


We have characterized the pancreatic phenotype of mice carrying a gene trap mutation in Sel1l. We show that Sel1l expression in the developing pancreas coincides with differentiation of the endocrine and exocrine lineages. Mice homozygous for the gene trap mutation die prenatally and display an impaired pancreatic epithelial morphology and cell differentiation. The pancreatic epithelial cells of Sel1l mutant embryos are confined to the progenitor cell state throughout the secondary transition. Pharmacological inhibition of Notch signaling partially rescues the pancreatic phenotype of Sel1l mutant embryos.


Together, these data suggest that Sel1l is essential for the growth and differentiation of endoderm-derived pancreatic epithelial cells during mouse embryonic development.