Fig. 1

Fig. 1 Cardiac morphogenesis in different genetic backgrounds. (A) Depiction of several key stages of zebrafish heart formation, beginning with the juxtaposition of two bilateral cardiac progenitor cell populations along the midline of the embryo (dotted line) to the elongation of the heart tube along the anterior-posterior axis. Dorsal view onto heart field. See text for detailed explanations. (B-I) cmlc2, (J,K) vmhc and (L,M) amhc expression. Embryos are 30-32 hpf. Parts L and M were captured with a 30° angle from dorsal for better visualization of atrial morphology. (B-D) Comparison of wild-type, has/prkci morphant and Tg(cmlc2:prkci) transgenic and has/prkci morphant embryos. (E) Heart cone formation is not completed, resulting in bilateral wings of myocardial progenitor cells (arrowheads) in prkci^2A kinase-dead mutants. (F,G) Heart cone `tilting' occurs, but heart tube elongation is delayed to varying degrees in nok mutants. (F) Severe and (G) medium-strength phenotypes. (H) nok/mpp5 morphants display a severe heart tube elongation defect. (I) Co-injection of nok/mpp5 MO with wild-type nok/mpp5 mRNA rescues myocardial morphogenesis. There is no developmental delay. (J,K) Length of the ventricle is affected in nok mutants. (L,M) Length of the atrium is shortened and, along the mediolateral axis, narrower than wild type. (N,O) nok^s305 mutants and embryos that express high levels of PRKCi^2A mutant protein (overexpression phenotype) are phenotypically similar. The body axis is curved ventrally and the retinal pigmented epithelium is largely disrupted, leaving the central portion of the retina uncovered, a phenotype more severe than in has mutants.