Fig. 4

Combined loss of Lef1 and Tcf7 does not recapitulate the pLL phenotype seen with the complete loss of Wnt signaling. (A-C) Zygotes from a lef1^nl2/+ incrosses were injected with tcf7-MO. NM distribution in the injected embryos was assessed by eya1 expression at 2 dpf and compared with uninjected lef1 mutant embryos. The loss of Tcf7 alone did not affect pLL patterning in lef1^nl2/+ sibling (A), the pLL is truncated more severely lef1^nl2/–; tcf7-MO (B; arrowhead) compared with lef1^nl2 mutants alone (C; arrowhead). Note reduced fin fold (black arrows) caused by a combined loss of Lef1 and Tcf7 as reported previously (Nagayoshi et al., 2008). (D) Axial positions of the pLL NMs (L1-L5) and primordium (mean±s.d.; n=11, P<0.001, two-way ANOVA with replication). (E-F′) pLL formation in 2 dpf embryos following the induction of Dkk1 in the Tg(hsp70l:dkk1-GFP) line by a heat-shock at 28 hpf. Position of the primordium at the time of heat-shock is marked by the yellow arrowheads. Dashed rectangles indicate the regions shown at higher magnification in E′,F′. Following the heat-shock, one or two NMs are deposited and the pLL ends with a trail of eya1-positive cells (white arrowheads). (G) Axial positions of NMs deposited following heat-shock in control and Tg(hsp70l:dkk1-GFP) embryos (n=11). Scale bars: 20 μm.