DEV012989 Supplementary Material

Files in this Data Supplement:

• Supplemental Figure S1 -

  Fig. S1. Dorsal neural cell number is increased in the chick spinal cord if either BMPRIA or BMPRIB are constitutively activated at HH stage 11/12. (A-H) CMV::caBMPRIA (A,B,E,F,I,J) or CMV::caBMPRIB (C,D,G,H,K,L) expression constructs were electroporated concomitantly with a control CMV::GFP vector into HH stage 11/12 embryos. Changes in cellular identity were examined in transverse sections of HH stage 19/20 spinal cords using antibodies against (A-D) pLh2 and (E-H) pIsl. For both dI1 and dI3 neurons, there was a significant increase in the number of cells on the electroporated compared with the non-electroporated sides of the spinal cord. (I-L) Labeling with phosSmad1/5/8 antibodies reveals that both CMV::caBMPRIA and CMV::caBMPRIB constructs are equally effective in activating the R-Smads at this stage of development (endogenous domain of phosSmad1/5/8 staining is indicated with an open arrowhead, I, K). Scale bar: 100 µm

• Supplemental Figure S2 -

  Fig. S2. Comparison of the percentage of mispolarized commissural axons in fillet preparations taken from different BMP and type I BMPR mutant embryos. The number of mispolarized axons in the Math1::cre; BmprIa^flox/flox; BmprIb^−/− double mutant fillets is statistically identical (P>0.4) to those in Gdf7^−/− fillets (Butler and Dodd, 2003).

• Supplemental Figure S3 -

  Fig. S3. Comparison of the reorientation angles of commissural axons growing in dorsal explants (d-sc) taken from the spinal cords of different BMP and type I BMPR mutant embryos. BmprIb^−/− commissural axons are reoriented by a rat RP to a statistically identical extent to the average reorientation angle of rat commissural axons responding to a RP deficient in either BMP7 (P>0.27) or GDF7 (P>0.28) (Butler and Dodd, 2003), suggesting that BMPRIB is the principle type I receptor that mediates the activity of the BMPs in the reorientation assay.