Fig. 6

The role of Her7 during pre-pattering.

Brightfield images of wild type and her7 mutant embryos at 16–18 somites (A, B). Compared to the wild type embryo (A), somite borders posterior to the 8^th somite are disrupted in the her7^hu2526 mutant (B, bracket). In situ hybridisation analysis of myoD expression (C, D), eplin (E, F), mespb (H, I) and mespb (J, K) in wild type and her7 mutants. Compared to half-segmental myoD expression in the wild type (C), myoD expression is disrupted posterior to the 8^th somite in her7^hu2526 mutants at 10–12 somites (D, bracket). In addition to the ALD at somite 8, her7^hu2526 mutant larvae show a PLD at around somite 17 (F, bracket indicates area of defect). eplin expression posterior to the PLD appears V-shaped as in wild-type at prim 6 stage (compare E, F). (G) graph plotting the number of her7^hu2526 embryos exhibiting defective somites (n = 56) as a function of their respective position along the a/p-axis of the animal. The obtained formula for the defect in the her7^hu2526 mutant is 8 (+/3)17 (+/3) indicating that in some rare cases the defects seem to appear at both the ALD and the PLD with a slight variability. mespb expression in the wild type and the her7^hu2526 mutant are shown in (H) and (I), respectively. (J) and (K) mespa expression in the wild type and her7^hu2526 mutant, respectively. Expression of both genes is disrupted in the her7^hu2526 mutant at 10–12 somite stage. (A, B, E, F) lateral view, anterior to the left; (C, D, H-K) dorsal view, anterior to the top.