Fig. 1

Fig. 1 Her1 mutants exhibit defects in somitogenesis.

Electropherogram of her1 (A) and her7 (B) amplicons in wild type (top), homozygous her1^hu2124 (bottom, A) and her7^hu2526 (bottom, B) mutant fish. Schematics above the sequences depict the exon- and intron-organization and the protein domains encoded by the exons. Point mutations are indicated by asterisks. (C, D) Brightfield pictures of wild type and her1 mutant embryos, lateral view, anterior to left. Compared to wild type embryos (C, asterisks), the first 3 somitic borders in the her1^hu2124 mutant appear diffuse and partly disrupted (D, bracket). In situ analysis of myoD expression in wild types indicates characteristic half-segmental expression within the somites (E, asterisks indicate somites 1–3). myoD expression is diffuse in the first 3 somites of her1^hu2124 embryos (F, bracket). (G, H) and (K, L) show half-segmental respectively r/c polarity wild type expression pattern of mespb at 10–12 somite stage and between 90% epiboly and bud stage, respectively. (I, J) and (M, N) represents mespb expression in the her1^hu2124 mutant at 10–12 somite stage and between 90% epiboly and bud stage, respectively. Expression of mespb is disturbed in the her1^hu2124 mutant between 90% epiboly and bud stage (M, N), when the anlagen of the first somites are pre-patterned. Compared to one or two stripes in the wild-type (K, L), mespb is expressed in a salt and pattern (M, N). mespb expression is unperturbed at 10–12 somite stage in her1^hu2124 mutants (I, J). Dorsal views, anterior to top.