The role of Her7 during pre-pattering.

<p>Brightfield images of wild type and <i>her7</i> mutant embryos at 16–18 somites (A, B). Compared to the wild type embryo (A), somite borders posterior to the 8<sup>th</sup> somite are disrupted in the <i>her7<sup>hu2526</sup></i> mutant (B, bracket). In situ hybridisation analysis of <i>myoD</i> expression (C, D), <i>eplin</i> (E, F), <i>mespb</i> (H, I) and <i>mespb</i> (J, K) in wild type and <i>her7</i> mutants. Compared to half-segmental <i>myoD</i> expression in the wild type (C), <i>myoD</i> expression is disrupted posterior to the 8<sup>th</sup> somite in <i>her7<sup>hu2526</sup></i> mutants at 10–12 somites (D, bracket). In addition to the ALD at somite 8, <i>her7<sup>hu2526</sup></i> mutant larvae show a PLD at around somite 17 (F, bracket indicates area of defect). <i>eplin</i> 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 <i>her7<sup>hu2526</sup></i> 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 <i>her7<sup>hu2526</sup></i> 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. <i>mespb</i> expression in the wild type and the <i>her7<sup>hu2526</sup></i> mutant are shown in (H) and (I), respectively. (J) and (K) <i>mespa</i> expression in the wild type and <i>her7<sup>hu2526</sup></i> mutant, respectively. Expression of both genes is disrupted in the <i>her7<sup>hu2526</sup></i> 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.</p>

Keyword(s)

License

CC BY 4.0