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Fig. 3. Attenuation of Disp1 activity in the Shh-producing notochord leads to a similar disruption of ventral neural tube patterning, as observed in Disp1 hypomorphic mutants. Sections through the neural tube of wild-type (A-E), Disp1 hypomorphic mutants (Disp1^2/2, Shh^+/-) (F-J), Disp1^C829F/2, Shh^+/- (P-T), and Disp1 conditional mutants [Disp1^2/2C, Shh^Cre (K-O) and Disp1^C829F/2C, Shh^Cre/+ (U-Y)]. In Disp1^2/2, Shh^+/- mutant (F-J): the floorplate is absent (F); Nkx2.2⁺ and Olig2⁺ cells are greatly reduced in number (G); Nkx2.2⁺ cells occupy the ventral midline (G); Nkx6.1⁺-positive cells are also affected (H); and the dorsal marker Pax7 is restricted to the dorsal domain (H). The conditional mutant Disp1^2/2C, Shh^Cre/+ maintains the early floorplate marker Foxa2 but no Shh expression is observed in the floorplate (K). Nkx2.2⁺ and Olig2⁺ cells are reduced in number to about 50% of the wild-type control levels and Nkx2.2⁺ cells occupy the ventral midline (L). In Disp1^2/C829F, Shh^+/- mutant (P-T), ventral progenitor cell numbers are further reduced compared with Disp1^2/2, Shh^+/-. No Nkx2.2⁺ cells are present (S) and the Pax7 and Pax6 domains move ventrally (R,S). Nkx2.2⁺ cells are still present in Disp1^C829F/2C, Shh^Cre/+ mutants (X).

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