Fig. 8. Myocardial gene expression responds to atrial dysfunction in wea mutants. (A-D) Lateral views at 96 hpf, anterior to the left. Whole-mount in situ hybridization compares expression of anf (A,B) and cmlc2 (C,D). Ventricle (V) and atrium (A) are indicated. Embryos were treated with 0.003% phenylthiourea from 24-96 hpf to inhibit pigmentation (Elsalini and Rohr, 2003). Embryos were sorted by phenotype prior to fixing, and tails were marked to distinguish between wild-type and wea mutant embryos. Mutant and wild-type siblings were then kept together throughout the in situ protocol, and were stained for the same length of time. (A,B) Comparison of wild-type (A) and wea mutant embryos (B) indicates substantial upregulation of anf expression throughout the wea mutant heart. (C,D) Likewise, the wea mutant heart exhibits upregulation of cmlc2 expression at this stage. Intensity of anf and cmlc2 expression is increased on a per cell basis; this is especially clear for the atrium, which is the same thickness in wild-type and wea mutant embryos.

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