Fig. 3

her3 and her9 expression is independent of Notch signaling. (A-L) Expression of neurod4 (A,E), her3 (B,F), her9 (C,G) and hes5 (D,G) in wild-type (A-D), mind bomb^m178 mutant (mib; E-H) and DAPT (γ-secretase inhibitor)-treated embryos (+DAPT; I-L) at the one-somite stage. Dorsal views with anterior towards the top. The expression of neurod4 became homogeneous within the proneuronal domains, and the expression of hes5 was abolished in the mib^m178 mutant and the DAPT-treated embryos. The expression of her3 and her9 was not affected in the mib^m178 mutant or the DAPT-treated embryos. (M-T) Expression of neurod4, her3, her9 and hes5 in embryos that had received an injection of β-galactosidase RNA (50 pg) and RNA for a constitutively active zebrafish notch5 (50 pg, +zN5ICD; M-P) or an antimorphic Xenopus Delta-1 (100 pg, +xDl^stu; Q-T) at the one-somite stage. Co-staining with the riboprobes and X-gal. Dorsal views with anterior towards the top. Misexpression of zN5ICD abolished the neurod4 expression and reduced the her3 expression at variable levels, and strongly induced the ectopic expression of hes5. By contrast, the expression of xDl^stu increased the neurod4 expression within the proneuronal domain and abolished the hes5 expression, but did not affect the her3 expression. The expression of her9 was not affected by the expression of either zN5ICD or xDl^stu.