Skip to main content
. Author manuscript; available in PMC: 2013 Aug 15.
Published in final edited form as: Dev Biol. 2012 Jun 12;368(2):382–392. doi: 10.1016/j.ydbio.2012.06.008

Figure 3. The schlei mutation rescues ventral neuronal specification in Shh pathway mutants.

Figure 3

e10.5 neural tubes stained for DAPI (blue) and neuronal markers (green). Expression of the dorsal marker Pax6, which is expanded in Shh (E) and Smo (C) mutants but absent in Ptch1 (A) is rescued and dorsally restricted in schlei-Ptch1 double mutants (B, bracket). In contrast, intermediate-level cells such as the Nkx6.1+ population and Olig2+ motor neuron progenitors, which require positive Shh signaling and are therefore absent in Shh and Smo, are able to form in schlei-Shh (F) and schlei-Smo (D) double mutants. These populations, which are expanded dorsally in Ptch1, are restored to a more ventral location in schlei-Ptch1 double mutants (arrows). High-level Shh targets (Nkx2.2+ V3 interneuron progenitors and Shh+ floorplate cells) are expanded dorsally in Ptch1 animals but are more ventrally restricted in schlei-Ptch1 double mutants (arrowheads). However, schlei is not able to rescue the loss of these cell types in Shh and Smo mutants. All neural tube sections are shown at the same magnification.