Fig. 2. Ablation of Bmpr1a in neural crest cells. We have used the Wnt1-Cre transgene to ablate Bmpr1a activity in mouse NCCs. In the mating scheme outlined here (A), one quarter of the resulting embryos cannot transduce signals through BMPRIA in the neural crest. (B) PCR primers designed to detect recombined Bmpr1a alleles from genomic DNA show recombination from 15 s embryos only in the presence of Cre. (C-F) At E11.0, wild-type and Wnt1-Cre; Bmpr1a^flox/null (mutant) embryos were morphologically indistinguishable. (G-J) Dissections at E11.5 showed an apparent lack of blood flow in mutant yolk sacs despite the presence of yolk sac blood vessels (I, arrows). Mutant embryos at E11.5 (J) show pooling of blood in peripheral vessels, heart, and liver. (K) Genotyping of dissected embryos reveals that Wnt1-Cre; Bmpr1a^flox/null embryos are fully represented (Mendelian expectation is 25%) until E12.5. At E12.5, half of embryos recovered are in the process of resorption (red) and half are clearly necrotic. No mutants have been recovered after E12.5.