Figure 9.

Inhibition of FGF signaling after cerebellar ablation impairs repatterning in the anterior hindbrain. A, B, Brightest point projection of z-stacks of 25 pictures from the cerebellum (lateral view) of gata1:GFP 781 strain embryos at 60 hpf recorded at a distance of 3 μm each by laser-scanning confocal microscopy. Inhibition of FGF signaling through administration of SU5402 from 36 to 60 hpf does not affect the induction or migration of GFP-expressing cerebellar neuronal cells (B), because they arise and migrate as in the cerebellum of untreated transgenic counterparts (A). C, D, Dorsal view of 72 hpf gata1:GFP 781 strain embryo stained by mRNA in situ hybridization for the expression of otx2 and hoxa2. Administration of SU5402 from 36 hpf until 60 hpf does not affect the spatiotemporal maintenance of both expression domains (C; compare with Fig. 6G). If the inhibitor treatment is preceded by surgical cerebellar ablation at 36 hpf, no repression of the hoxa2 expression close to the new MHB, as found after cerebellar ablation alone (compare with Fig. 6H), can be observed (D). SU5402 treatment from 36 hpf until 60 hpf does not affect zic1 expression at 72 hpf (E; compare with Fig. 4E). However, when SU5402 is administered after cerebellar ablation, the reexpression of zic1 in a mediolateral stripe along the new MHB indicative for cerebellar regeneration (F; compare with Fig. 4F) is inhibited. cb, Cerebellum; mes, mesencephalon; rh, rhombencephalon.