Fig. 9. Summary of the changes in neuronal fate in Olig3 mutant mice. Summary of the neuronal types generated in the alar plate of control and Olig3 mutant mice in (A) rhombomeres 4-6 and (B) rhombomere 7. In Olig3 mutant mice, the fate of class A neurons was not correctly determined, and ectopic Lbx1⁺ neurons appear instead. (C) Model of Olig3 function in fate determination of dA4 climbing fiber neurons. Olig3 and Ptf1a cooperate to induce the dA4 fate; Olig3 exerts its function primarily by suppressing Lbx1. Ptf1a is known to suppress Tlx3 (Glasgow et al., 2005; Mizuguchi et al., 2006; Hori et al., 2008), and the dA4 fate might require the suppression of Lbx1 and Tlx3 by Olig3 and Ptf1a, respectively. Olig3 also appears to suppress Ptf1a; it should be noted that in normal development, Olig3 and Ptf1a are only transiently co-expressed in cells that locate to the border of the ventricular zone (VZ) and mantle zone (MZ). The colors indicate the neuronal subtypes defined in Fig. 1I by their transcription factor code.