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Fig. 5. Characterization of myocardial defects observed in Wnt11-R-depleted embryos. In all cases, myocardial tissue is detected by in situ hybridization using MHCα probe. (A–D) One-sided injection of either contMO (A and B) or Wnt11-R MO1 (C and D) does not interfere with myocardial differentiation when assayed at st. 28. (E–F) Control MO-injected embryos assayed at st. 34 showing normal expression of MHCα when viewed laterally (E), ventrally (F), or in section G. (H–K) MO1-injected embryos assayed at st. 34 showing myocardial marker expression in lateral (H) and ventral (I) views. Sectioning of embryos through the heart region (J and K) shows abnormal morphology of the heart tube. (L–N) Isolated hearts assayed at st. 45. Normal heart morphology is illustrated in L and abnormal, partially bilaterally duplicated hearts from Wnt11-R-depleted embryos are shown in M and N. Atria (a), ventricle (v), and outflow tracts (oft) are indicated. (O) Section through the heart tube of a st. 34 embryo injected with MO1 on one side, as indicated. (P) Same section as O showing detection of cell nuclei using propidium iodide staining under UV light. The myocardial layer is outlined. Nuclei were counted to assay cell number in Wnt11-R-depleted and -untreated myocardial tissue. |
