Fig. 5.

Defects in proteoglycan and ECM distribution are not the primary cause of LR abnormalities in Sox17 mutants. Co-IHC of chondroitin sulfate, laminin and GFP in Sox17^GFP/+ and Sox17^GFP/GFP mouse embryos at 3-4 ss. The Sox17^GFP allele is a null mutation. Chondroitin sulfate (proteoglycan) and laminin (ECM) are distributed uniformly in Sox17^GFP/+ embryos (A-A″), whereas Sox17^GFP/GFP embryos showed either regional defects (B-B″, stars in B′; n=7/17) or almost normal phenotypes (C-C″; n=10/17) in the organization of chondroitin sulfate and laminin. Ect, ectoderm; Mes, mesoderm.