Notochord repression of endodermal Sonic hedgehog permits pancreas development
AUTOR(ES)
Hebrok, Matthias
FONTE
Cold Spring Harbor Laboratory Press
RESUMO
Notochord signals to the endoderm are required for development of the chick dorsal pancreas. Sonic hedgehog (SHH) is normally absent from pancreatic endoderm, and we provide evidence that notochord, in contrast to its effects on adjacent neuroectoderm where SHH expression is induced, represses SHH expression in adjacent nascent pancreatic endoderm. We identify activin-βB and FGF2 as notochord factors that can repress endodermal SHH and thereby permit expression of pancreas genes including Pdx1 and insulin. Endoderm treatment with antibodies that block hedgehog activity also results in pancreatic gene expression. Prevention of SHH expression in prepancreatic dorsal endoderm by intercellular signals, like activin and FGF, may be critical for permitting early steps of chick pancreatic development.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=316875Documentos Relacionados
- Notochord induction of zebrafish slow muscle mediated by Sonic hedgehog
- Short- and long-range effects of Sonic hedgehog in limb development
- Pancreas development is promoted by cyclopamine, a Hedgehog signaling inhibitor
- Sonic hedgehog-dependent activation of Gli2 is essential for embryonic hair follicle development
- Multiphasic and tissue-specific roles of sonic hedgehog in cloacal septation and external genitalia development