Fig. 7
Ztcf7l1a-/- mutants lacking Hesx1 function fail to form eyes.
(A) Schematic of the genetic strategy to isolate mutations that modify the tcf7l1a-/- mutant phenotype. (B–C) U910 modifier of the tcf7l1a-/- mutant phenotype. Lateral views of homozygous U910 embryos that are heterozygous (B) or homozygous (C) for the tcf7l1amutation. (D) Representation of SSLP segregation linkage analysis mapping of U910 modifier of tcf7l1a to a 1.46 megabase (Mb) interval on chromosome 11 (Ch11; rec, recombinants). (E) RT-PCR for hesx1 spanning exons 1–2 (top panel), exons 2–3 (middle panel) and β-actin (bottom panel) on wildtype (lanes 1 and 2) and U910-/- (lanes 3 and 4) embryo cDNA from 1 cell stage (lanes 1 and 3) and 10hpf (lanes 2 and 4). Single experiment. (F–I) hesx1 in situhybridisation on wildtype (F–H) and U910-/- (I) embryos at epiboly (ep) stages indicated. Dorsal views, anterior up. (J, K) Lateral views of hesx1-/- (Δex1/2)/tcf7l1a+/- (J) and hesx1-/-(Δex1/2)/Ztcf7l1a-/- (K) embryos. Four independent experiments, n = 53. Scale bars = 200 µm.