Fig. 4

Cdx-deficient embryos have patterning defects in the pLPM. In situ hybridizations for scl-1 (A, B) tbx5a (D–E) and hand2 (G, H) at 14 hpf as well as tbx5a (I–J) and fgf24 (K, L) at 18 hpf. (A, B) Wt and Cdx-deficient embryos are comparable in the AP length of scl-1. (C) Quantification of the AP length of scl-1 (black bracket, A) normalized to the trunk width for wt and Cdx-deficient embryos. Expression of tbx5a relative to the eye is unaffected between wt and Cdx-deficient embryos (D, E). (F) Quantification of the AP length between tbx5a in the aLPM and the eye (bracket, D) shown as a ratio of the distance between the aLPM and the anterior eye, normalized to the width of the trunk, is comparable between wt and Cdx-deficient embryos. (G, H) The expression length of hand2 in the pLPM is reduced in Cdx-deficient embryos (black arrowheads, H) compared to expression in wt (white arrowheads, G). (I, J) Expression of tbx5a at 18 hpf is expanded posteriorly in the pLPM of Cdx-deficient embryos (black arrowheads, J), compared to wt (white arrowheads, I). (K, L) Expression of fgf24 at 18 hpf is expanded along the AP axis in Cdx-deficient embryos to somite levels 2–4 (black arrowheads, L) compared to wt where fgf24 is expressed at the level of somites 2–3 (white arrowheads, K). Embryos are oriented in a dorsal view (A–B, D–E, I–L) or laterally with the anterior end towards the left (G-H). Non-significant differences in the quantitative analysis are indicated as NS. Scale bars represent 100 μm.