Fig. 11.

Model to explain motor neuron phenotypes of dtr (gli1⁻) and yot (gli2^DR) mutants, and of gli1, gli2, and gli3 morpholino injection experiments. The hindbrain and spinal cord are shown schematically in lateral view (anterior is to left), with the branchiomotor and spinal motor neurons depicted as black ovals. Rhombomeres 2–7 (r2–r7) and the caudal hindbrain (chb) are indicated. The pathways depict signaling within ventral neural tube cells upon transduction of Hh signal through the Smoothened (Smo, black rectangle)-Patched (Ptc, black triangle) receptor system. In the hindbrain, Hh-mediated induction of motor neurons (and motor neuron markers like nk2.2, islet1, and tag1) is completely dependent on gli1 function. Branchiomotor neuron loss in yot mutants appears to result from the action of mutant Gli2 (Gli2^DR) on Gli1 activator function. Complete activation of net1a and ptc1 expression requires activator function of Gli1, Gli2, and Gli3. In the spinal cord, Gli1, Gli2, and Gli3 activator functions contribute to spinal motor neuron induction (and islet1 and tag1 marker gene expression). The significant loss of spinal motor neurons in yot mutants appears to result from the dominant repressor effect of Gli2^DR on all Gli activators. Gli1 expression in the hindbrain and spinal cord appears to specifically require Gli3 activator function.