Silencing of TGF-β signalling by the pseudoreceptor BAMBI

Darya Onichtchouk, Ye-Guang Chen, Roland Dosch, Volker Gawantka, Hajo Delius, Joan Massague´ () and Christof Niehrs ()
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Darya Onichtchouk: Divisions of Molecular Embryology
Ye-Guang Chen: Memorial Sloan-Kettering Cancer Center and Howard Hughes Medical Institute
Roland Dosch: Divisions of Molecular Embryology
Volker Gawantka: Divisions of Molecular Embryology
Hajo Delius: Applied Tumor Virology, Deutsches Krebsforschungszentrum
Joan Massague´: Memorial Sloan-Kettering Cancer Center and Howard Hughes Medical Institute
Christof Niehrs: Divisions of Molecular Embryology

Nature, 1999, vol. 401, issue 6752, 480-485

Abstract: Abstract Members of the transforming growth factor-β (TGF-β) superfamily, including TGF-β, bone morphogenetic proteins (BMPs), activins and nodals, are vital for regulating growth and differentiation1. These growth factors transduce their signals through pairs of transmembrane type I and type II receptor kinases2,3,4. Here, we have cloned a transmembrane protein, BAMBI, which is related to TGF-β-family type I receptors but lacks an intracellular kinase domain. We show that BAMBI is co-expressed with the ventralizing morphogen BMP4 (refs 5, 6) during Xenopus embryogenesis and that it requires BMP signalling for its expression. The protein stably associates with TGF-β-family receptors and inhibits BMP and activin as well as TGF-β signalling. Finally, we provide evidence that BAMBI's inhibitory effects are mediated by its intracellular domain, which resembles the homodimerization interface of a type I receptor and prevents the formation of receptor complexes. The results indicate that BAMBI negatively regulates TGF-β-family signalling by a regulatory mechanism involving the interaction of signalling receptors with a pseudoreceptor.

Date: 1999
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DOI: 10.1038/46794

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