Fig. 1

Effects of the whz mutation on embryonic heart morphology and growth.

(A-D) Lateral view of wild-type (wt; A, C) and whz mutant (B, D) embryos at 72 hours post fertilization (hpf). Whz mutants show pericardial edema, blood congestion at the cardiac inflow tract and stretched heart chambers. (E, F) Hematoxylin and Eosin staining of sagittal histological sections of wt (E) and whz mutant (F) hearts at 72 hpf. Similar to wild-types, in whz atria and ventricles, myocardial (myo) and endocardial (endo) cell layers are clearly defined and separated by an atrio-ventricular canal (AVC). In contrast to wild-type hearts, whz mutant ventricles appear small and the myocardium monolayered. (G-I) Dissected wt (G) and whz mutant (H) hearts at 72 hpf, stained with a cardiomyocyte-specific MEF-2 antibody (nuclei; red) and co-stained with S46, exclusively marking atrial cardiomyocytes (green). (I) whz mutant hearts show significantly reduced ventricular cardiomyocytes at 72 hpf (sib: 144.2±10 SD and whz: 94.9±10 SD, n = 10; p<0.0001), whereas cardiomyocyte numbers are comparable between wt and whz ventricles at 48 hpf (wt: 93.4±10 SD and whz: 88.2±10 SD, n = 10; p>0.05).