Fig. 2

Fig. 2 Loss of FoxD5 function resulted in loss of somite polarity during somitogenesis. The FoxD5-MO1-injected embryos with abnormal phenotypes were categorized as having severe defects, such as smaller head size and distortion axis (B), and mild defects, such as reduced head and disordered somites with irregular boundary (C). Dorsal views of trunk somites in WT embryos (WT; D) and FoxD5-MO1-injected embryos (E, F) at 18 hpf. In WT embryos, column-shaped, maturely formed somites (indicated by black arrowheads) and two newly forming somites S-I and S-II (blue arrowheads) were observed. Meanwhile, in FoxD5 morphants, wider and more raggedly formed mature somites (black arrowheads) and newly forming somites, but with irregular somitic furrows (red arrowhead), were observed. The expressions of cb1045 at 18-hpf in WT embryos and FoxD5 morphants were also studied. The cb1045 was specifically observed in the somite borders of WT embryos (G), but it was lost in FoxD5 morphants (H). Co-injection of FoxD5-MO1 and tFoxD5 mRNA enabled embryos to rescue the defective expression of cb1045 induced by FoxD5-MO1 alone (I). In vivo HOM sectioning of WT embryos (J–L) and FoxD5 morphants (M–O) at 24 hpf was examined under bright field (J, M) and dark field microscopes (K, L, N, O). The morphological structures, including skin and somite boundaries, which are labeled in purple, were observed by third harmonic generation signal, whereas muscle fibers, which are labeled in green, were observed by second harmonic generation emissions. Compared to the WT embryos (K, L), the structure of the somites in the FoxD5 morphants was disordered (N, O).