Fig. 7

Fig. 7 Cdx-deficiency results in a caudal shift in aldh1a2 expression as well as a caudal expansion of cyp26a and hoxd4a at the tailbud stage (A–F). In situ hybridization for aldh1a2 (A–B), cyp26a (C–D), at the tailbud stage and hoxd4a at 1-2ss (E–F). Expression of aldh1a2 relative to the notochord shifts caudally in Cdx-deficient embryos (black arrowhead, B), compared to wt (white brackets, A). The length between the anterior boundary of aldh1a2 and the notochord (white brackets) was quantified and normalized to the yolk diameter (G). Expression of cyp26a in the trunk mesoderm was compared relative to expression in the anterior neuroectoderm (C, D). The rostral boundary of cyp26a in the trunk was unaffected in Cdx-deficient embryos (D) compared to wt (C), although the posterior boundary of cyp26a expanded caudally. The length between cyp26a in the trunk mesoderm and neuroectoderm (white bracket in C) was quantified and normalized to the yolk diameter (H) and no significant differences were observed. Expression of hoxd4a expanded caudally in Cdx-deficient embryos (black arrowhead, F), compared to wt (E). (I) Diagram of the presumed RA distribution (blue) relative to Cyp26a and the fin field (green) in wt and Cdx-deficient embryos at the tailbud stage. Embryos are shown in dorsal view, anterior to the top and dashed lines indicate the threshold between low and high levels of RA. Statistical significance was calculated by using the student t-test, (*, p < 0.05). Non-significant differences are indicated as NS. Scale bar represents 100 μm.