DEV01349 Supplementary Material

Files in this Data Supplement:

• Supplemental Figure 1 -

  Fig. S1. Loss of expression of Hh downstream targets at E9. (a-f) Coronal sections of an E9 (14-17 somite) wild-type (a,c,e) and Smo^c/–;Foxg1^Cre mutant (b,d,f) telencephalon. Normal expression of Gli1 (a) is absent from the Smo^c/–;Foxg1^Cre mutant (b), indicating that Hh signaling is removed ventrally by E9. Nkx2.1 expression, shown just after its initiation in the wild-type telencephalon at E9 (e), is never found in the Smo^c/–;Foxg1^Cre mutant telecephalon (f). c and d show the extent of telencephalic fate with Foxg1 staining.

• Supplemental Figure 2 -

  Fig. S2. Cell-autonomous requirement of Hh signaling for ventral telencephalic patterning. (a-d) Coronal sections of an E10.5 Smo null chimera, where null cells are marked by expression of b-gal. (b) An adjacent section where Nkx2.1 expression is shown through in situ hybridization, pseudo-colored in red. (c) High-power view of area shown in a, where lacZ staining is pseudo-colored in green. (d) Digital overlay of sections shown in b and c, showing the complimentary expression of b-gal and Nkx2.1.