Activin receptor patterning of foregut organogenesis
Document Type
Article
Abstract
Foregut development produces a characteristic sequence of gastrointestinal and respiratory organs, but the signaling pathways that ensure this developmental order remain largely unknown. Here, mutations of activin receptors ActRIIA and ActRIIB are shown to disrupt the development of posterior foregut-derived organs, including the stomach, pancreas, and spleen. Foregut expression of genes including Shh and Isl1 is shifted in mutant mice. The endocrine pancreas is particularly sensitive to the type and extent of receptor inactivation. ActRIIA(+/-)B(+/-) animals lack axial defects, but have hypoplastic pancreatic islets, hypoinsulinemia, and impaired glucose tolerance. Thus, activin receptor-mediated signaling regulates axial patterning, cell differentiation, and function of foregut-derived organs.
Keywords
Activin, Diabetes mellitus, Endoderm, Foregut, Hedgehog, Pancreas
Publication Date
9-2-2000
Publication Title
Genes and Development
ISSN
08909369
Volume
14
Issue
15
First Page
1866
Last Page
1871
PubMed ID
10921901
Recommended Citation
Kim, Seung K.; Hebrok, Matthias; Li, En; Oh, S. Paul; Schrewe, Heinrich; Harmon, Erin B.; Lee, Joon S.; and Melton, Douglas A., "Activin receptor patterning of foregut organogenesis" (2000). Translational Neuroscience. 715.
https://scholar.barrowneuro.org/neurobiology/715