Int. J. Dev. Biol. 55: 45 - 58 (2011)

https://doi.org/10.1387/ijdb.103158sp

Vol 55, Issue 1

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

Original Article | Published: 1 February 2011

Sabine Pfister¹, Vanessa J. Jones¹, Melinda Power¹, Germaine L. Truisi¹, Poh-Lynn Khoo¹, Kirsten A. Steiner¹, Masami Kanai-Azuma², Yoshiakira Kanai³, Patrick P. L. Tam^1,4 and David A. F. Loebel^1,4,5

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.

Keywords

Sox17, downstream gene, endoderm, heart morphogenesis