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Notochord repression of endodermal Sonic hedgehog permits pancreas development
M Hebrok1, S K Kim, D A Melton
1Department of Molecular and Cellular Biology and Howard Hughes Medical Institute, Harvard University, Cambridge, Massachusetts 02138 USA.
Genes & Development
|June 17, 1998
Summary
Notochord signaling is crucial for chick dorsal pancreas development. It represses Sonic hedgehog (SHH) in endoderm, allowing pancreas gene expression and development.
Area of Science:
- Developmental biology
- Endocrinology
- Molecular biology
Background:
- Notochord signaling is essential for chick dorsal pancreas formation.
- Sonic hedgehog (SHH) is typically absent in pancreatic endoderm.
- The notochord's role in regulating SHH in pancreatic endoderm is unclear.
Purpose of the Study:
- To investigate the role of notochord signals in regulating SHH expression in chick pancreatic endoderm.
- To identify specific notochord factors involved in this regulation.
- To understand how SHH repression by the notochord permits pancreatic gene expression.
Main Methods:
- Analyzing gene expression in chick embryos.
- Using antibodies to block hedgehog signaling.
- Identifying notochord-derived signaling molecules (activin-betaB, FGF2).
Main Results:
- Notochord represses SHH expression in adjacent pancreatic endoderm.
- Activin-betaB and FGF2 from notochord inhibit endodermal SHH.
- Blocking hedgehog activity promotes pancreatic gene expression (Pdx1, insulin).
Conclusions:
- Notochord-derived signals, including activin and FGF, are critical for repressing SHH in early pancreatic development.
- SHH pathway inhibition by intercellular signals is essential for initiating chick pancreatic development.