Supplementary Materials

Supplementary Materials for:

A Wnt-Bmp Feedback Circuit Controls Intertissue Signaling Dynamics in Tooth Organogenesis

Daniel J. O'Connell, Joshua W. K. Ho, Tadanori Mammoto, Annick Turbe-Doan, Joyce T. O'Connell, Psalm S. Haseley, Samuel Koo, Nobuhiro Kamiya, Donald E. Ingber, Peter J. Park, Richard L. Maas*

*To whom correspondence should be addressed. E-mail: maas{at}genetics.med.harvard.edu

This PDF file includes:

  • Text S1. Quality assessment of microarray data.
  • Text S2. Comparison with qualitative gene expression data from the BITE-IT database.
  • Text S3. Construction of a gene regulatory network from perturbation data.
  • Text S4. Simulation of the Wnt-Bmp feedback circuit.
  • Fig. S1. LCM workflow.
  • Fig. S2. Principal components analysis of time series gene expression profiles.
  • Fig. S3. Analysis of gene expression concordance between epithelium and mesenchyme with the LCM and manually dissected time course data sets.
  • Fig. S4. Average scaled gene expression patterns of different signaling pathway components.
  • Fig. S5. Expression dynamics of representative extracellular signaling molecules and receptors (Bmp, Wnt, Fgf, and Shh pathways).
  • Fig. S6. Heat maps of average expression of cellular components in different signaling pathways.
  • Fig. S7. A schematic illustration of the construction of a molecular concept map.
  • Fig. S8. Molecular concept maps showing significant overlap between various sets of differentially regulated genes.
  • Fig. S9. Epithelial and mesenchymal gene regulatory networks reconstructed using our probabilistic method.
  • Fig. S10. An expanded view of the Wnt-Bmp feedback circuit.
  • Fig. S11. Constitutive canonical Wnt signaling induces supernumerary tooth development in the absence of Pax9.
  • Fig. S12. Coronal sections of molar regions from control, Pax9-null, epithelial Apc loss-of-function, and compound epithelial Apc loss-of-function; Pax9-null mutants at E14.0.
  • Fig. S13. Constitutive canonical Wnt signaling induces supernumerary tooth formation in the absence of Msx1.
  • Fig. S14. Coronal sections of molar regions from control, Msx1-null, epithelial Apc loss-of-function, and compound epithelial Apc loss-of-function; Msx1-null mutants at E14.0.
  • Fig. S15. Constitutive canonical Wnt signaling fails to induce tooth formation in the absence of epithelial Bmpr1a.
  • Fig. S16. qRT-PCR expression analysis at E14.5 in the isolated epithelium of epithelial Apc loss-of-function and of compound epithelial Apc loss-of-function; Bmpr1a loss-of-function mutants.
  • Fig. S17. Coronal sections of molar regions from control, epithelial Apc loss-of-function, epithelial Bmpr1a loss-of-function, and compound epithelial Apc loss-of-function; Bmpr1a loss-of-function mutants at E14.0.
  • Table S1. Comparison of BITE-IT and microarray data from this study.
  • Table S2. Gene sets used in this study.
  • Table S3. Custom gene sets used in this study.

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Citation: D. J. O'Connell, J. W. K. Ho, T. Mammoto, A. Turbe-Doan, J. T. O'Connell, P. S. Haseley, S. Koo, N. Kamiya, D. E. Ingber, P. J. Park, R. L. Maas, A Wnt-Bmp Feedback Circuit Controls Intertissue Signaling Dynamics

in Tooth Organogenesis. Sci. Signal. 5, ra4 (2012).

© 2012 American Association for the Advancement of Science