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. 2002 May;22(9):3149–3156. doi: 10.1128/MCB.22.9.3149-3156.2002

FIG. 2.

FIG. 2.

AP-2γ-deficient embryos are severely retarded in development. (A) Whole-mount in situ staining for the primitive streak marker Brachyury (T) of a wild-type conceptus (right) and an AP-2γ-deficient conceptus (left) at E8.0 of murine development. The blue staining indicates cells expressing Brachyury (arrows). (B to E) Histological sections of wild-type (wt) and AP-2γ-deficient (−/−) embryos in utero at E7.5 of murine development. Sagittal section through the decidua (dc) harboring a wild-type (B) and an AP-2γ-deficient embryo (C). Note the reduced size of the ectoplacental cone in panel C compared to that in panel B (epc; arrow). PCNA staining of wt conceptus (D) and AP-2γ-deficient (−/−) conceptus (E) at E7.5 of development. Note the difference in proliferation (red signal) in the ectoplacental cone and in the extraembryonic ectoderm for the wild-type conceptus and for the mutant. Arrowheads mark erythrocytes corresponding to forming blood lacunas indicative of the beginning of resorption of the mutant conceptus. Abbreviations: hf, head fold; wt, wild type; dc, decidua; epc, ectoplacental cone. Scale bars, 500 μm (A to C) and 100 μm (D and E).