Fig. 3. ash1a and ngn1 are important regulators of neurogenesis in the epiphysis. A-F and I-L are dorsal views of the epiphysis with anterior at the top. G and H are lateral views of the brain with anterior to the right. (A-F) Expression of isl1 at the 25-somite stage in the epiphysis of wild-type (WT), ash1a MO-, ash1a^5'UTR MO-, ngn1MO-, ash1a and ash1a^5'UTRMO-, or ash1a and ngn1 MO-injected embryos. Neuronal production was reduced in ash1a morphants (B,C,E) but was normal in the ngn1 morphant (D). A stronger effect was observed in the double ash1a/ngn1 morphant (F) compared with single ash1a morphants (B,C,E). A combination of ash1a^5'UTR MO and ash1a MO gave rise to a similar phenotype (E) to the single ash1a or ash1a^5'UTR morphants (B,C). (G,H) Expression of isl1 at 25 hours in the heads of wild-type and ash1a-morphant embryos. The black arrowhead indicates the nucleus of the posterior commissure and the white arrow indicates the adenohypophysis (G); both are sites where isl1 expression is disrupted in the ash1a morphant (H). A reduction of the number of neurones was observed in the epiphysis of the ash1a morphant (H). By contrast, structures in which ash1a is not expressed, like the trigeminal ganglia, are not affected in the ash1a morphant. (I,J) Expression of ngn1 in wild-type and ash1a-morphant embryos at the 20s stage. (K,L) Expression of ash1a in wild-type and ngn1-morphant embryos at the 17s stage. Hy, hypothalamus; Tg, trigeminal ganglia. Scale bars: in A, 10 µm for A-F,I-L; in H, 50 µm for G,H.