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.
  

[Download PDF]

Technical Details

Format: Adobe Acrobat PDF

Size: 4.64 MB

© 2012 American Association for the Advancement of Science