Fig. 7. Ectopic cell death correlates with the loss of ectopic nuclei by 14.5 dpc. (A,B) TUNEL staining in parasagittal sections of wild-type and Hoxb1 mutant hindbrains. There was ectopic cell death in the mutant (B, black arrowheads) caudally to the pontine flexure (pf). (C-F) Pial (ventricular where noted) views of Isl1 expression in wild-type (C), Hoxa1 (D), Hoxb1 (E) and Hoxb2 (F) mutant flat-mounted hindbrains at 13.5 dpc. By this stage, VIIm had normally completed their migration (C, black arrowheads). In Hoxa1 mutants, a small VIIm of variable size could be detected (D, black arrowheads), whereas the VIm was absent (D, white arrowheads). In Hoxb1 mutants, ectopic nuclei could still be detected (E, asterisks). The VIIm (E, white arrowheads), but not the VIm (E, black arrowheads) were absent. In Hoxb2 mutants, ectopic nuclei could also be detected (F, asterisks), whereas the VIm and a small VIIm were present (F, black arrowheads). (G-J) Pial (ventricular where noted) views of Isl1 expression in wild type (G), Hoxa1 (H), Hoxb1 (I) and Hoxb2 (J) mutant flat-mounted hindbrains at 14.5 dpc. In the wild type, Isl1 expression persisted in the Vm, VIm and VIIm (G, black arrowheads). In Hoxa1 mutants, the VIIm were either missing or rudimentary (H, white and black arrowheads), whereas the VIm was absent (H, white arrowheads). In Hoxb1 and Hoxb2 mutants, no ectopic nuclei could be detected. The VIIm was absent in Hoxb1 mutants (I, white arrowheads) and reduced in Hoxb2 mutants (J, black arrowheads), while the VIm was present in both mutants (I,J, black arrowheads).

Return to article