Fig. 3. Defects in extraembryonic tissue development of the Ldb1 mutant. (A,B) Benzidine staining reveals development of a network of blood islands and primitive vessels (arrow) in the wild-type conceptus at E8.5 (A), which do not exist in the Ldb1^-/- mutant (B). (C,D) Alkaline phosphatase staining of a wild-type and a mutant E7.5 conceptus, respectively. Primordial germ cells at the base of the allantois are stained in the control (arrow in C, magnified in the inset), while this signal is absent in the mutant (D). (E,F) Extraembryonic tissue morphology. The mesodermal and ectodermal layers (arrow) of the amnion are properly extended at the embryonic/extraembryonic junction of a wild-type embryo (E). During its outgrowth the allantois maintains contact with the embryonic tissue (large arrow in E). In the Ldb1^-/- mutant embryo (F) the ectodermal layer (arrowhead) of the amnion fails to expand, thus creating a contriction at the embryonic-extraembryonic junction. Although the mesodermal layer of the amnion is expanded, it fails to extend at the constricted embryonic/extraembryonic junction and forms pockets at the anterior and posterior ends (small arrows in F). The mutant allantois (large arrow in F) appears to have lost contact with the embryonic tissue.