Fig. 5

Molecular markers define an early axial patterning defect in β4GalT1 morphant embryos. (A–E) Control and β4GalT1MO embryos at 80–90% epiboly. (F–J) Control and β4GalT1MO embryos at the mid-somite stage. In situ hybridization for ntl (A) and cyc (B) shows shortened and widened expression domains in β4GalT1MO embryos. (C) In situ hybridization for PAPC marks the lateral mesoderm, illustrating a wider and more irregular axial domain (bracket) than in control embryos. (D) her1 in situ hybridizations reveal that fgf signaling is occurring in the lateral mesoderm, but the axial mesoderm interface is irregular, as seen with PAPC. (E) kny expression is retained in the evacuated zone (bracket indicates the evacuated zone) suggesting a defect in convergent extension. (F) ntl expression continues to be truncated in 10-somite β4GalT1MO embryos, and shows severe undulation. (G) MyoD expression is retained in the adaxial cells (arrowheads) of β4GalT1MO embryos, whereas expression in the somitic mesoderm is markedly reduced relative to control embryos. (H–J) Patterning of the somitic mesoderm and central nervous system appear relatively normal in β4GalT1MO embryos as indicated by her1 (H) and EphA4 (I, J) expression, respectively, although the somitic mesoderm is more diffuse and the notochord retains its undulating appearance, as seen with ntl.