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Fig. S2

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ZDB-IMAGE-071204-1
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Figures for Jazwinska et al., 2007
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Fig. S2 SB431542 and SB505124 Cause the Same Embryonic Phenotype as Overexpression of a Dominant-Negative Alk4 Receptor. Embryos were analyzed 3 days after fertilization. (A) Wild-type. (B) The transgenic embryos hsp:Alk4DN-GFP carry a construct with the coding sequence of the zebrafish alk4 receptor with a point mutation to replace highly conserved lysine K234 with arginine that is predicted to delete kinase function. The gene is fused to green fluorescent protein (GFP) and it is cloned under heat-shock-protein 70 promoter [S3]. For the induction of the expression of the construct, embryos were heat-shocked at 38°C for 1 hr at shield stage. (C and D) Embryos were treated with 50 μM SB431542 (Alk4-i) (C) and 2 μM SB505124 (D) starting at the two-cell stage. The morphological defects caused by the overexpression of a dominant-negative Alk4 receptor and inhibitor treatment are the same: the reduction of the head size, eye fusion or cyclopia, and perturbations of the body axis. This phenotype was highly penetrant, with 80% to 90% of embryos (n = 100) showing significant defects.

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