FIGURE

Fig. S2

ID

ZDB-FIG-071204-9

Publication

Jazwinska et al., 2007 - Activin-betaA Signaling Is Required for Zebrafish Fin Regeneration

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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.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	zf54Tg
Condition:	heat shock
Observed In:	eye head whole organism
Stage:	Protruding-mouth

Phenotype Detail

Acknowledgments

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