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Knockdown of VE-cadherin causes defective cardiac looping and chamber thinning. In situ hybridization of Control MO and VE-cad MO injected embryos with the pan-cardiac myosin marker cmlc2 (a–h) and the ventricular-specific vmhc (i–j). Ventral and lateral images of control embryos stained for cmlc2 (a,c) show proper atrial (white arrow) and ventricular (black arrows) looping. Images of VE-Cad knockdown embryos show a linear arrangement of the cardiac chambers (b,d). By 96 hours, cmlc2 staining shows the normal side-by-side arrangement of chambers in control embryos (e,g), while the heart remains thinned and tubular in VE-cad MO injected embryos (f,h). Staining for vmhc at 72 hours shows a compact ventricular chamber in controls (i), while the ventricles of knockdown embryos are elongated and thinner-appearing (j).
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