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doi:10.1534/genetics.106.064956
A more recent version of this article appeared on November 1, 2006.
REGULAR RESEARCH PAPERS |
dSno facilitates Baboon signaling in the Drosophila brain by switching the affinity of Medea away from Mad and toward dSmad2
Norma Takaesu 1, Cathy Hyman-Walsh 2, Ling Ye 3, Robert Wisotzkey 1, Michael Stinchfield 1, Michael O'Connor 3, David Wotton 2 and Stuart J. Newfeld 1*
1 Arizona State University
2 University of Virginia
3 University of Minnesota
* To whom correspondence should be addressed. E-mail: newfeld{at}asu.edu.
Submitted on August 17, 2006
Revised on August 21, 2006
Accepted on 21 August 2006
A screen for modifiers of Dpp adult phenotypes led to the identification of the Drosophila homolog of the Sno oncogene (dSno). The dSno locus is large, transcriptionally complex and contains a recent retrotransposon insertion that may be essential for dSno function, an intriguing possibility from the perspective of developmental evolution. dSno is highly transcribed in the embryonic central nervous system and transcripts are most abundant in third instar larvae. dSno mutant larvae have proliferation defects in the optic lobe of the brain very similar to those seen in baboon (Activin Type I receptor) and dSmad2 mutants. This suggests that dSno is a mediator of Baboon signaling. dSno binds to Medea and Medea/dSno complexes have enhanced affinity for dSmad2. Alternatively, Medea/dSno complexes have reduced affinity for Mad such that in the presence of dSno Dpp signaling is antagonized. We propose that dSno functions as a switch in optic lobe development - shunting Medea from the Dpp pathway to the Activin pathway to insure proper proliferation. Pathway switching in target cells is a previously unreported mechanism for regulating TGF
signaling and a novel function for Sno/Ski family proteins.
Key Words:
Drosophila, Smad genes, Sno oncogene, TGF signaling, developmental evolution
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