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. Author manuscript; available in PMC: 2016 Jul 1.
Published in final edited form as: Dev Biol. 2015 Apr 20;403(1):80–88. doi: 10.1016/j.ydbio.2015.04.008

Fig. 3. Inactivation of Wnt3 in the visceral endoderm leads to delayed formation of the primitive streak.

Fig. 3

A, B. Lateral views of control (A) and Wnt3 VE-null (VE-KO) (B) embryos hybridized with T. The vertical lines in B, indicate the length of the epiblast (a) and primitive streak (b) as indicated by T expression. C. Analysis of the extent of primitive streak development between control (Wnt3c/c) and VE-KO (Wnt3c/c;TtrCre/0) embryos. A comparison of the ratio of the extent of T expression relative to the proximodistal length of the epiblast (as indicated in B) reveals significant delay in the development of the primitive streak in VE-KO embryos relative to controls (p<0.001). D. Chimera derived from a tetraploid Wnt3 null (Wnt3lacZNeo/Δ3,4) blastocyst injected with R26lacZ ES cells. Embryo is composed solely of ES cells and has undergone gastrulation, indicating that Wnt3 function in the visceral endoderm is dispensable for gastrulation. The yolk sac appears blue due to the presence of β-gal positive extra-embryonic mesoderm cells derived from the R26lacZ ES cells. h, head; vys, visceral yolk sac. E – G. Lateral (E) and posterior (F) views of control (Wnt3c/Δ3,4) and Wnt3-VE mutant embryos heterozygous for Wnt3 in the epiblast (VE-KO*; Wnt3c/Δ3,4;TtrCre/0) hybridized with T at E6.5 (E and F) and E7.5 (G). The Wnt3c/Δ3,4;TtrCre/0 embryo fails to elongate the anteroposterior axis at E6.5 and has abnormal gastrulation at E7.5 as shown by the presence of a bulge of cells in the primitive streak (arrow), failure to close the proamniotic canal (arrowhead) and absence of T staining in axial mesoderm (asterisk). Panels A and B and E and F are shown at the same scale. Scale bars, 100 μm in B and F, 500 μm in D, and 200 μm in G.