Silencing expression of progesterone receptor (PGR) in uterine epithelia is a prerquisite for implantation in mammals. Therefore, progesterone (P4) acts via PGR-positive uterine stromal cells to increase expression of progestamedins, e.g. fibroblast growth factor-7 (FGF7) and FGF10, as well as hepatocyte growth factor (HGF) in sheep uteri. The progestamedins, as well as interferon tau (IFNT) exert paracrine effects on uterine epithelia and conceptus trophectoderm that express receptors for FGF7 and FGF10 (FGFR2IIIb) and HGF (MET) to stimulate cell signaling pathways including phosphatidyl inositol kinase 3 kinase (PI3K) and mitogen activated protein kinase (MAPK) to stimulate gene expression and secretory responses by trophectoderm and uterine luminal (LE) and superficial glandular (sGE) epithelia that do not express signal transducers and activators of transcription (STAT1/STAT2). Thus, IFNT activates undefined alternate cell signaling pathways that may include PI3K and MAPK to influence gene expression by uterine LE and sGE.