Fig. 5. wea^m58 and wea^sk7 are strong loss-of-function alleles of amhc. (A) The wea^m58 mutation is a deletion of a single T at position 4024 of the amhc orf, which creates a frame-shift (arrow points to the position of the missing T). (B) The wea^sk7 mutation is a T to A substitution at position 4577 of the amhc orf, which creates a premature stop codon (arrow points to the mutation). (C) Both mutant amhc cDNAs are predicted to encode truncated Amhc proteins. The wild-type Amhc protein contains 1937 amino acids, the predicted wea^m58 Amhc protein would contain 66 missense amino acids (gray bar) and would terminate after amino acid 1407, and the predicted wea^sk7 Amhc protein would terminate after amino acid 1524. (D-F) Lateral views at 48 hpf, anterior to the left, of whole-mount immunofluorescence with MF20 (TRITC) and S46 (FITC). Ventricle (V) and atrium (A) are indicated. Phenotype of wild-type (D) and wea mutant embryos (E) is as described in Fig. 3. Embryos injected with an anti-amhc morpholino (F) exhibit a phenotype indistinguishable from that of wea mutant embryos (E). 138/138 morpholino-injected embryos phenocopy the wea mutation, and 120/120 embryos injected with a control morpholino appear wild type. Note that the wea mutant ventricle (E) and the morpholino-injected ventricle (F) both appear smaller than the wild-type ventricle (D).