Fig. 4
Figure 4. Nkd1 does not rescue the hdl/tcf7l1a mutant.
Homozygous deletion of tcf7l1a results in an eyeless phenotype due to activated canonical Wnt signaling (D). Overexpression of Nkd1 in embryos from a homozygous hdl-/- parental cross (B, E) does not rescue the eyeless phenotype (E) and does not affect development of the early embryo (B), although at 1 dpf, nkd1 injected embryos typically have a kinked axis. Injection of nkd1 MO into embryos from a hdl +/- X hdl -/- parental cross has no affect on early (C) or 1 dpf (F) development (Uninj hdl +/- n= 14, hdl -/-n= 16; Nkd1 MO injected hdl +/- n= 15, hdl -/-n=22). Experiments in embryos from homozygous hdl-/- parental crosses had similar results (not shown).