Figure 4

Ptc1;ptc2 double mutants show mediolateral and anteroposterior somite patterning defects. Patterning of adaxial cells and slow muscle cell precursors is disturbed in ptc1;ptc2 mutants. The region of myod positive adaxial cells and eng1 expressing slow muscle precursors are expanded at 19 hpf (A-D). At 19 hpf, prdm1 expression is highly induced in the ptc1;ptc2 mutant, suggesting that the myotome is mainly developing slow muscle type precursors (E,F). Anteroposterior patterning of the somites is lost in segmented somites, since the posterior somite marker uncx4.1 (G,H) and anterior somite marker fgf8 (I,J) are strongly reduced or not detectable at 19 hpf. myf5 expression in 11 somite stage wildtype (K,L) and ptc1;ptc2 double mutant embryos (M,N). L and N are higher magnification of relevant areas of K and M, respectively. In wild type, myf5 is expressed at higher levels in the posterior of the somites during their formation, in more posterior (younger) segments this appears to include the adaxial cells (*). In more anterior (more mature) somites more anterior adaxial cells appear to show higher levels of labeling (arrowheads). In ptc1;ptc2 double mutant embryos (N) a "salt and pepper" type staining suggests that anterior and posterior cells are intermingled. Additionally, dlc necessary for proper segmentation is present in presomitic mesoderm but failed to be expressed in the posterior part of segmented somites (O,P), suggesting that somite formation and A/P patterning of formed somites are genetically uncoupled processes.