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. 2017 Apr 1;144(7):1249–1260. doi: 10.1242/dev.147322

Fig. 2.

Fig. 2.

Targeted deletions of proximal enhancers show that only the VPE is required for proper gastrulation. (A) Targeted deletions of the 5 kb ΔPSE, 2 kb ΔPSE_b and 0.7 kb ΔVPE generated by homologous recombination (Figs S2-S4). (B) Whole-mount in situ hybridisation of EomesΔVPE/− embryos. Class I mutants exhibit failure in A-P axis specification; class II display APS defects. At E6.5 in class I mutants, expression of the AVE marker Hex is confined to the distal VE (n=4/10 EomesΔVPE/− embryos analysed). At E7.5, the mesoderm marker Brachyury (n=2/5) and the DE marker Foxa2 (n=3/7) are mislocalised proximally. In class II mutants, Hex marks the AVE, Brachyury expression fails to extend distally (n=3/5), whereas the Foxa2 domain is confined to the APS and the DE domain is lost (n=3/7). Consistent with failure to specify DE in both mutant classes, expression of Afp+ VE cells fails to disperse proximally (for class I and class II, n=2 and n=2 out of 7 EomesΔVPE/− embryos analysed, respectively). At E9.5, class II mutants display venture closure and neural tube defects, fused or malformed somites, loss of Otx2+ forebrain tissue and an anterior truncation of the Shh midline (n=3/3 viable morphologically abnormal EomesΔVPE/− embryos recovered). Scale bars: 100 μm.