Successful implantation in mammals depends critically on the establishment of a receptive environment in the uterus and on reciprocal and synchronized interactions between uterine and embryonic tissues (for reviews, see (1,2)). A suitable maternal environment for implantation is established and strictly regulated by the combined action of estrogen and progesterone, being initiated by a nidatory pulse of estrogen acting on a uterus already prepared by progesterone. Prior to implantation, the uterus undergoes dramatic morphologic changes in response to estrogen from ovarian follicles and progesterone from corpora lutea. The requirement for progesterone in priming the uterus is demonstrated by hormone deprivation in which the blastocysts remain in a state of diapause, a suspended state of low metabolism, and only after endometrial preparation by progesterone has been completed is estrogen effective in inducing a state of receptivity (reviewed in (11)). A second surge of estrogen secreted from the ovarian follicles just prior to implantation triggers the start of implantation. Lactation or ovariectomy eliminates this estrogen surge and prevents the attachment reaction and the blastocysts remain in a delayed implantation state (3). Although the molecular mechanisms responsible for implantation remain unclear, targeted mutagenesis in mice has implicated one subfamily of mammalian homeobox genes, the Abdominal B (AbdB) Hox genes, as important components of the implantation mechanism.
