Int. J. Dev. Biol. 55: 45 - 58 (2011)
doi: 10.1387/ijdb.103158sp
© UBC Press

Sox17-dependent gene expression and early heart and gut development in Sox17-deficient mouse embryos

Sabine Pfister1, Vanessa J. Jones1, Melinda Power1, Germaine L. Truisi1, Poh-Lynn Khoo1, Kirsten A. Steiner1, Masami Kanai-Azuma2, Yoshiakira Kanai3, Patrick P. L. Tam1,4 and David A. F. Loebel1,4,5

1Embryology Unit, Children’s Medical Research Institute, New South Wales, Australia, 2Center for Experimental Animals, Tokyo Medical and Dental University, Tokyo, Japan, 3Department of Veterinary Medicine, University of Tokyo, Tokyo, Japan and 4Sydney Medical School, University of Sydney, New South Wales, Australia

ABSTRACT Sox17 is a transcription factor that is required for maintenance of the definitive endoderm in mouse embryos. By expression profiling of wild-type and mutant embryos and Sox17-overexpressing hepatoma cells, we identified genes with Sox17-dependent expression. Among the genes that were up-regulated in Sox17-null embryos and down-regulated by Sox17 expressing HepG2 cells is a set of genes that are expressed in the developing liver, suggesting that one function of Sox17 is the repression of liver gene expression, which is compatible with a role for Sox17 in maintaining the definitive endoderm in a progenitor state. Consistent with these findings, Sox17-/- cells display a diminished capacity to contribute to the definitive endoderm when transplanted into wild-type hosts. Analysis of gene ontology further revealed that many genes related to heart development were downregulated in Sox17-null embryos. This is associated with the defective development of the heart in the mutant embryos, which is accompanied by localised loss of Myocd-expressing cardiogenic progenitors and the malformation of the anterior intestinal portal.


Sox17, downstream gene, endoderm, heart morphogenesis

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