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Figure 3


Fig. 3. ALK5 knock-in mice show an embryonic lethality similar to ALK5–/– but express PSMAD1 protein. (A,B) Embryos from conventional ALK5–/– mice (KO) die in mid-embryogenesis. At E9.5, the yolk sac from ALK5–/– mice shows impaired blood vessel development when compared with yolk sac from wild-type (WT) mice (arrow). The embryos exhibit cardiac effusion (arrowheads). (C,D) Similarly, ALK5(D266A) knock-in (KI) embryos show defects in the yolk sac and in heart development. (E-J) PSMAD1 (PS1) and PSMAD2 (PS2) were detected by immunohistochemistry in both the endothelial (EC, black arrowhead) and mesothelial (mes, red arrowhead) cell layer of wild-type (E,F), ALK5–/– (G,H) and ALK5(D266A) knock-in (I,J) yolk sacs. In the yolk sac from ALK5–/– mice, PSMAD1 was not detected in the endothelial layer (G), but PSMAD2 was observed (H). Scale bars, 0.5 mm.





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