Distinct mesodermal signals, including BMPs from the septum transversum mesenchyme, are required in combination for hepatogenesis from the endoderm.
By J. M. Rossi, N. R. Dunn, B. Hogan, K. Zaret. Genes & Development, 2001
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Mesodermal signaling is critical for patterning the embryonic endoderm into different tissue domains. Classical tissue transplant experiments in the chick and recent studies in the mouse indicated that interactions with the cardiogenic mesoderm are necessary and sufficient to induce the liver in the ventral foregut endoderm. Using molecular markers and functional assays, we now show that septum transversum mesenchyme cells, a distinct mesoderm cell type, are closely apposed to the ventral endoderm and contribute to hepatic induction. Specifically, using a mouse Bmp4 null mutation and an inhibitor of BMPs, we find that BMP signaling from the septum transversum mesenchyme is necessary to induce liver genes in the endoderm and to exclude a pancreatic fate. BMPs apparently function, in part, by affecting the levels of the GATA4 transcription factor, and work in parallel to FGF signaling from the cardiac mesoderm. BMP signaling also appears critical for morphogenetic growth of the hepatic endoderm into a liver bud. Thus, the endodermal domain for the liver is specified by simultaneous signaling from distinct mesodermal sources.
Subfields: Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/6bbca6808a600dcb57af7ae0919f6fd1335b2c19
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Citations in the corpus
- Organogenesis and development of the liver. (2010, background): “expression of the secreted bone morphogenetic protein, BMP4 (Nemer and Nemer, 2003), which, like GATA4, is highly expressed in the septum transversum mesenchymal cells at the eight somite stage of mouse development (Rossi et al., 2001).”
- Pancreas organogenesis: From bud to plexus to gland (2011, background): “BMPs positively regulate the endodermal expression of GATA4, and act in parallel to cardiac-derived FGFs in the induction of liver fate (Rossi et al., 2001) (Fig.”