Fig. 1. Foxh1 is essential for ASE activity in vivo. (A) The 600 ASE deletion was engineered in the context of both the wild-type and Nodal^LacZ loci, resulting in the Nodal⁶⁰⁰ and Nodal^600.LacZ alleles, as indicated. The PEE, Node and ASE enhancers are indicated by colored circles, and the exons by black boxes. (B-I) ß-Galactosidase staining patterns in 6.5 dpc embryos with anterior towards the left. (B) Wild-type (WT) embryos express the ASE lacZ transgene in the epiblast (more strongly in the posterior than the anterior) and overlying VE. (C) By contrast, the ASE lacZ transgene is not expressed in Foxh1-deficient embryos. (D) Nodal^LacZ is expressed in the epiblast and overlying VE of WT embryos. By contrast, in Foxh1-deficient embryos (E), expression is proximally restricted within the epiblast and lost from the overlying VE. (F) A proportion (25%) of Foxh1^–/–, Nodal^LacZ/+ embryos show a more severe phenotype, are rounded in appearance with a uniformly thickened VE, and display ß-galactosidase staining throughout the epiblast but not in the VE. (G) Nodal^600.LacZ/+ embryo showing expression confined to the proximal posterior epiblast, and undetectable in the VE. (H) In Foxh1^–/– embryos, Nodal^600.LacZ expression is similarly restricted to the proximal epiblast but lacks AP asymmetry. (I) A rare Foxh1^–/–, Nodal^600.LacZ/+ embryo, with a more severe phenotype showing ß-galactosidase staining throughout the epiblast. PEE, posterior epiblast element; ASE, asymmetric element; Node, node-specific enhancer.

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