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Dlx5  and  Dlx6  are two closely associated homeobox genes which code for transcription factors involved in the control of steroidogenesis and reproduction. Inactivation of  Dlx5 / 6  in the mouse results in a Leydig cell defect in the male and in ovarian insufficiency in the female.  DLX5/6  are also strongly expressed by the human endometrium but their function in the uterus is unknown. The involvement of  DLX5/6  in human uterine pathology is suggested by their strong downregulation in endometriotic lesions and upregulation in endometrioïd adenocarcinomas. We first show that  Dlx5 / 6  expression begins in Müllerian ducts epithelia and persists then in the uterine luminal and glandular epithelia throughout post-natal maturation and in the adult. We then use a new mouse model in which  Dlx5  and  Dlx6  can be simultaneously inactivated in the endometrium using a  Pgr cre/+   allele. Post-natal inactivation of  Dlx5 / 6  in the uterus results in sterility without any obvious ovarian involvement. The uteri of  Pgr cre/+  ;  Dlx5/6 flox/flox   mice present very few uterine glands and numerous abnormally large and branched invaginations of the uterine lumen. In  Dlx5/6  mutant uteri, the expression of genes involved in gland formation ( Foxa2 ) and in epithelial remodelling during implantation ( Msx1 ) is significantly reduced. Furthermore, we show that DLX5 is highly expressed in human endometrial glandular epithelium and that its expression is affected in endometriosis. We conclude that  Dlx5  and  Dlx6  expression determines uterine architecture and adenogenesis and is needed for implantation. Given their importance for female reproduction,  DLX5  and  DLX6  must be regarded as interesting targets for future clinical research.

Dlx5 and Dlx6 control uterine adenogenesis during post-natal maturation: possible consequences for endometriosis