Figure 4: The knockdown of has2 or tbx5a alleviates the heart defect in kctd10 mutants.
(a–f) The MO against has2 or tbx5a was injected into the embryos derived from the in-cross of Tg(cmlc2:EGFP)+/34c fish. The heart of the kctd10 mutant (d) was markedly smaller than the wild-type embryos (a) at 48 hpf. The AVC of wt embryos injected with has2 MO became wider (b), and the heart of wt embryos injected with tbx5a MO is slightly shrunken (c). (e,f) Some injected mutants have nearly normal cardiac morphogenesis. (g–l) In situ hybridization of has2 in the mutants injected with tbx5a MO. Has2 was expressed in the very restricted region of the endocardium in wild-type embryos (g, arrow), whereas it expanded throughout the endocardium of the heart tube in the kctd10 mutants (h). When treated with 3 ng of tbx5a MO, the ectopic expression of has2 decreased moderately in some mutants (i); in case of injection with 5 ng of tbx5a MO, has2 was undetectable in wild-type embryo (j), but restricted at the AVC in 5/16 mutants (k, arrow); in 3/16 mutants, has2 disappeared (l). All the embryos used here were genotyped. Ventral views with the anterior at the top. (a–f) Scale bar=0.1 mm; (g–l) Scale bar=0.1 mm.
