FIG. 3.

The nuclear protein-binding site is required for in vivo activity of the mouse flk1 promoter in transgenic mouse embryos. (A) Representative whole-mount β-galactosidase-stained E11.0 embryos. Transgenic mouse embryos expressing β-galactosidase under control of the flk1 promoter-enhancer stain the vascular endothelium diffusely and strongly. In contrast, a 5-bp mutation within the nuclear protein-binding site identified by footprinting resulted in the loss of β-galactosidase expression in most transgenic embryos. (B) Summary of in vivo activity of the wild-type and mutant transgenic constructs.