Fig. 4

Knockdown of the dvr1 gene leads to abnormal C&E movements. (A–H) Whole-mount in situ hybridization for fgf8a, dlx3b, ctsl1b, myod1 and ntla were performed in control and dvr1 mo^ATG morphants at the indicated developmental stages. (I–P) Whole-mount in situ hybridization for ntla, dlx3b, ctsl1b, egr2b and myod1 were performed in control and dvr1 mo^SB morphant embryos at the indicated developmental stages. The percentage of phenotypes were as follows: (J) 17/19 (ntla), (L) 42/44 (dlx3b), 13/44 (ctsl1b), (N) 23/25 (egr2b), (P) 34/34 (myod1). Red double-headed arrows denote the width of the presumptive hindbrain in the lateral view or the width of rhombomeres 3 and 5 in the dorsal view. Green dotted lines indicate the angle between the two sides of the neural plate. Black and blue double-headed arrows show the width and length of somites in E-F and O-P, respectively. Black double-headed arrows in I and J indicate the length of the notochord. Embryos were dorsal view in left side of A-B, E-F, I-J and M-P with head to the top, animal view in C-D and K-L with head to the left, lateral view in right side of A and B with head to the top, lateral view in left side of G and H and dorsal view in right side of G and H with head to the left. (Q) The C&E defects were specifically caused by Dvr1 inhibition. Whole-mount mRNA in situ hybridization of the expression pattern of myod1 in control, dvr1 mo^ATG-injected and dvr1 mo^ATG plus dvr1 mRNA-injected embryos at 9-somite stage.