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Sci. Signal., 11 October 2011
[DOI: 10.1126/scisignal.2002034]

Supplementary Materials for:

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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Format: Adobe Acrobat PDF

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Citation: E. Eivers, H. Demagny, R. H. Choi, E. M. De Robertis, Phosphorylation of Mad Controls Competition Between Wingless and BMP Signaling. Sci. Signal. 4, ra68 (2011).

© 2011 American Association for the Advancement of Science


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