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Fig. S6
Subtle enhancement of the nkx2.5 mutant phenotype by treatment with a low dose of SU5402. (A-D) In situ hybridization depicts frontal views of amhc expression in wild-type (A,B) and nkx2.5 homozygous mutant (C,D) embryos at 48 hpf. Embryos were treated with DMSO (A,C) or 4 μm SU5402 (B,D) from 18 hpf until 30 hpf. In wild-type embryos, this relatively low dose of SU5402 altered cardiac morphology but did not induce ectopic amhc-expressing cells (B). However, in a few nkx2.5 mutants, this dose of SU5402 resulted in the increased presence of ectopic amhc in the ventricle (arrowhead, D); this example is representative of 9 similar embryos observed in a total of 135 progeny from 4 independent intercrosses of nkx2.5 heterozygotes. This subtle enhancement of the nkx2.5 mutant phenotype (C) suggests that FGF signaling may act in the same pathway as the nkx genes to repress the inappropriate expression of amhc. Scale bar: 50 μm.