Hgs homozygous mutant embryos develop with their ventral region outside of the yolk sac, have two independent bilateral heart tubes (cardia bifida), lack a foregut, and die around embryonic day 11 (E11.0). These phenotypes arise from a defect in ventral folding morphogenesis that occurs normally around E8.0. Significant apoptosis is detected in the ventral region of mutant embryos within the definitive endoderm, suggesting an important role for this germ layer in ventral folding morphogenesis. Abnormally enlarged early endosomes are detected in the mutants in several tissues including definitive endoderm, suggesting that a deficiency in vesicular transport via early endosomes underlies the mutant phenotype. The vesicular localization of Hgs is disrupted in cells treated with wortmannin, implicating Hgs in the phosphatidylinositol 3-kinase pathway of membrane trafficking.

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These Hgs knock-out mice exhibit development with the ventral region outside of the yolk sac, two independent bilateral heart tubes, lack of a foregut, and die around embryonic day 11. They are suitable for use in applications related to the study of vesicular trafficking.

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