Drosophila Dpp signaling is mediated by the punt gene product: A dual ligand-binding type II receptor of the TGFβ receptor family

Anthea Letsou, Kavita Arora, Jeffrey L. Wrana, Karl Simin, Vern Twombly, Joumana Jamal, Karen Staehling-Hampton, F. Michael Hoffmann, William M. Gelbart, Joan Massagué, Michael B. O'Connor

Research output: Contribution to journalArticlepeer-review

239 Scopus citations


Signaling by TGFβ-related factors requires ligand-induced association between type I and type II transmembrane serine/threonine kinases. In Drosophila, the saxophone (sax) and thick veins (tkv) genes encode type I receptors that mediate signaling by decapentaplegic (dpp), a member of the bone morphogenetic protein (BMP) subgroup of TGFβ-type factors. In this report, we demonstrate that the Drosophila punt gene encodes atr-II, a previously described type II receptor that on its own is able to bind activin but not BMP2, a vertebrate ortholog of dpp. Mutations in punt produce phenotypes similar to those exhibited by tkv, sax, and dpp mutants. Furthermore, punt will bind BMP2 in concert with tkv or sax, forming complexes with these receptors. We suggest that punt functions as a type II receptor for dpp and propose that BMP signaling in vertebrates may also involve sharing of type II receptors by diverse ligands.

Original languageEnglish (US)
Pages (from-to)899-908
Number of pages10
Issue number6
StatePublished - Mar 24 1995

Bibliographical note

Funding Information:
We thank Dr. J. Wozney for BMP2, S. Lin for construction of the ubi-punf P element, and Ft. Warrior and L. Attisano for many helpful discus- sions. This work was supported by grants from the March of Dimes Birth Defects Foundation and the American Cancer Society to A. L. and by grants from the Public Health Service to F. M. H., W. M. G., and M. B. 0. This work was also supported by grants from the National Institutes of Health to J. M. and to the Memorial Sloan-Kettering Cancer Center. J. L. W. is a Medical Research Council of Canada postdoctoral fellow. J. M. is a Howard Hughes Medical Institute Investigator.


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