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. 2000 Feb 1;105(3):261–270. doi: 10.1172/JCI8856

Figure 5.

Figure 5

Failure of vascular smooth muscle differentiation in dHAND mutants. Mesenchymal cells in wild-type (a) and dHAND mutants (b) expressed the mesenchymal marker, COUPTFII, throughout the embryo. Expression of lacZ under the control of the SM-22α promoter was seen in the aortic arch arteries (aa), aorta (ao), conotruncus (ct), and ventricle (v) of the heart of an E9.5 transgenic embryo (c). In the dHAND-null background, the SM-22-lacZ transgene expressed in the atrium (a) of the heart, but not in the vasculature (d) at E9.5. Embryos are shown in lateral views focusing on the cardiac and vascular areas. Histologic analysis of wild-type (e) and mutant (f) embryos revealed absence of lacZ expression in the cells surrounding the aorta in dHAND-null embryos. Electron microscopy of transverse sections through the rostral part of E9.5 wild-type (g) and dHAND-null (h) embryos revealed vascular mesenchymal (m) cells surrounding endothelial (e) cells. Wild-type mesenchymal cells developed cytoplasmic processes to contact endothelial cells, whereas dHAND-null mesenchymal cells remained rounded without contacting endothelial cells.