DEV000729 Supplementary Material

Files in this Data Supplement:

• Supplemental Figure S1 -

  Fig S1. Defective eye formation and cleft secondary palate in hypomorphic Shh^flox/− mutants. (A-C) Hematoxylin and Eosin-stained representative coronal sections through the eyes of E12.5 wild-type (A) Shh^flox/− (B) and ShhN/− (C) mouse embryos. Note the abnormally thickened and distorted neural retina, as well as the degenerated lens (B,C, arrows). (D,E) Hypomorphic Shh^flox/− mutant develops cleft secondary palate at E18.5 (E). Note the opposed and closed palatal shelves and maxillary bones in the wild type (D), in contrast to widely open palatal shelves and defective residual maxillary bones in Shh^flox/− (E). nr, neural retina; l, lens; m, maxillary bones; ps, palatal shelves.

• Supplemental Figure S2 -

  Fig. S2. Dorsal ventral patterning in ShhN/− at E9.5. (A-H) Pax7 and Nkx6.1 expression in wild type (A-D) and ShhN/− (E-H). As shown in the bar chart (I), the Pax7 domain in ShhN/− spinal cord was moderately expanded, whereas the p0/p1 domain was moderately reduced. Note the comparable neural tube size at this stage. (J) Spinal cord size comparison between wild type and ShhN/− at E10.5. D, relative length along dorsoventral axis; d, relative length along left-right axis. S, approximate relative spinal cord size.

• Supplemental Figure S3 -

  Fig. S3. Shh expression in E10.5 wild-type and ShhN/− spinal cord. Shh immunohistochemistry revealed indistinguishable staining pattern between E10.5 wild-type (A) and Shh^+/− (B) spinal cord.