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. 2000 Jan 4;97(1):320–324. doi: 10.1073/pnas.97.1.320

Figure 3.

Figure 3

Comparison of whole-mount X-Gal staining of KZ26 +/− and KZ26 −/− chimeric embryos. ES cells with one (KZ26 +/−) or two (KZ26 −/−) Lmo2 null alleles were injected into C57/BL6 blastocysts and transferred to recipient females. At the indicated embryonic days, embryos were excised and whole-mount stained with X-Gal to test for β-galactosidase activity caused by Lmo2–lacZ gene expression. (A) E11.5 KZ26 +/− chimeric embryo with a staining pattern similar to that seen in heterozygous KZ26 mice. (B) E11.5 KZ26 −/− chimeric embryo derived from KZ26 −/− clone 1. In this embryo, ES cell contribution (blue) can be seen in the hippocampus and limb buds, and very few endothelial cells are stained blue (i.e., those of ES cell origin). (C) E12.5 KZ26 +/− chimeric embryo. Like the E11.5 KZ26 +/− embryo, the staining pattern was very similar to that seen in heterozygous KZ26 mice. (D–F) E12.5 KZ26 −/− chimeric embryos of three independent −/− clones. (D) An embryo derived from injection of KZ26 −/− clone 1. (E) An embryo from clone 16. (F) An embryo from clone 64. In KZ26 −/− chimeric embryos after E11.5, there was no contribution of −/− ES cells in endothelial cells of major vessels, whereas expression is maintained in the hippocampus, the limb bud, and tail. This selective loss of ES contribution in blood vessel endothelium suggests an essential role of Lmo2 protein in the maturation of vascular network (angiogenesis).