Open Close
Reference
Citation
Wisotzkey, R.G., Mehra, A., Sutherland, D.J., Dobens, L.L., Liu, X., Dohrmann, C., Attisano, L., Raftery, L.A. (1998). Medea is a Drosophila Smad4 homolog that is differentially required to potentiate DPP responses.  Development 125(8): 1433--1445.
FlyBase ID
FBrf0102610
Publication Type
Research paper
Abstract

Mothers against dpp (Mad) mediates Decapentaplegic (DPP) signaling throughout Drosophila development. Here we demonstrate that Medea encodes a MAD-related protein that functions in DPP signaling. MEDEA is most similar to mammalian Smad4 and forms heteromeric complexes with MAD. Like dpp, Medea is essential for embryonic dorsal/ventral patterning. However, Mad is essential in the germline for oogenesis whereas Medea is dispensable. In the wing primordium, loss of Medea most severely affects regions receiving low DPP signal. MEDEA is localized in the cytoplasm, is not regulated by phosphorylation, and requires physical association with MAD for nuclear translocation. Furthermore, inactivating MEDEA mutations prevent nuclear translocation either by preventing interaction with MAD or by trapping MAD/MEDEA complexes in the cytosol. Thus MAD-mediated nuclear translocation is essential for MEDEA function. Together these data show that, while MAD is essential for mediating all DPP signals, heteromeric MAD/MEDEA complexes function to modify or enhance DPP responses. We propose that this provides a general model for Smad4/MEDEA function in signaling by the TGF-beta family.

PubMed ID
PubMed Central ID
DOI
Associated Information
Comments
Associated Files
Other Information
Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Development
    Title
    Development
    Publication Year
    1987-
    ISBN/ISSN
    0950-1991
    Data From Reference
    Aberrations (10)
    Alleles (17)
    Gene Groups (1)
    Genes (11)
    Physical Interactions (1)
    Insertions (2)
    Transgenic Constructs (5)