Fig. 6

Fig. 6 Knockdown of kapd decreases the transcript levels of markers of immature and mature DA neurons in the ventral diencephalon at 18 hpf. (A-F) WISH analysis with nkx2.2- and olig2-specific probes detected reduction in their transcripts in the ventral diencephalon at 18 hpf. (A) WT embryo, (B) 5-mismatch MO control, and (C) kapd MO (0.2 ng of kapd morpholino per embryo). (G-L) WISH analysis of kapd MO (0.2 ng of kapd morpholino per embryo) using otx2b and th as probes. (G) otx2b transcripts in the midbrain of WT embryos at 18 hpf. (H) Embryos injected with 5-mismatch showed similar patterns to those of WT embryos. (I) kapd MO shows remarkable reduction of otx2b transcripts in the midbrain including midbrain ventricle at 18 hpf. Transcripts of th in WT (J), 5-mismatch control (K), and kapd MO (L) at 18 hpf. th transcripts were present in the ventral diencephalon in WT and 5-mismatch control whereas the expression was lost in the corresponding areas of kapd morphants. (M-O) Embryos were examined for the expression of neural crest marker, zic2b at 18 hpf. Transcripts of zic2b in WT (M) and 5-mis MO control (N). Injection of kapd MO caused notable reduced zic2b expression domains, ventral diencephalic and mesencephalic region at 18 hpf (O). (A-O) Scale bars = 100 μm.