Fig. 1. Morphological and molecular defects are similar among a class of zebrafish mutants. (A-E) Lateral views of live embryos at 36 hours post-fertilization (hpf), anterior towards the left. All embryos are depicted at the same magnification. Compared with wild-type embryos (A), pan (B), sk8 (C) and s30 (D) mutants exhibit reduced pigmentation, short tails, small ears and pericardial edema. s30;pan double mutants (E) exhibit a more extreme phenotype, including a shorter tail and neural cell death. (F-U) Whole-mount in situ hybridization indicates expression of gata4 (F-I), nkx2.5 (J-M) or cmlc2 (N-U); dorsal views of embryos, anterior towards the top. At 13 hpf (eight-somite stage), expression of gata4 and nkx2.5 are comparable in wild-type embryos (F,J), pan mutants (G,K) and s30 mutants (H,L); however, expression is reduced in s30;pan double mutants (I,M). At 16.5 hpf (15-somite stage), wild-type embryos (N) exhibit robust expression of cmlc2 in differentiating myocardiocytes, but pan mutants (O), s30 mutants (P) and s30;pan double mutants (Q) all lack cmlc2 expression. By 26 hpf, wild-type embryos (R) form a cmlc2-expressing heart tube, and pan mutants (S) generate a small and variable number of disorganized myocardiocytes (Yelon et al., 1999), but cmlc2 remains undetectable in s30 mutants (T) and s30;pan double mutants (U).