Phosphorylation of Mad Controls Competition Between Wingless and BMP Signaling

Edward Eivers, Hadrien Demagny, Renee H. Choi, Edward M. De Robertis*

*To whom correspondence should be addressed. E-mail: ederobertis{at}mednet.ucla.edu

This PDF file includes:

• Fig. S1. Increased BMP signals generated by a stabilized Mad protein.
• Fig. S2. Mad-GM8 expression increases the area of Distalless, a downstream target of Wg.
• Fig. S3. Inducible RNAi directed against Wg depletes Wg protein and its downstream target Senseless.
• Fig. S4. Mad-GM8 expression in the eye imaginal disc produces phenotypes suggestive of high Wg signaling.
• Fig. S5. C-terminal phosphorylation of Mad enables BMP4 to repress the Mad-induced increase in Tcf reporter gene activity.
• Fig. S6. The Mad RNAi phenotype is rescued by coexpression of a human Smad1 transgene.
• Fig. S7. Mad is required for Wg signal transduction during wing margin development.
• Fig. S8. Inhibition of GSK3 activity by BIO enhances the binding of Mad to Pangolin.
• Table S1. Primer sequences.
• References

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© 2011 American Association for the Advancement of Science