Liver X Receptor α (LXRα) Regulates 5β‐Reductase (AKR1D1) Expression in Avian Embryos: Implications for Yolk Steroid Metabolism

Steroid-mediated maternal effects are well-studied as a source of phenotypic variation. In bird eggs, the yolk contains various steroids that can influence embryonic development. However, one complicating factor in understanding how yolk steroids affect development is that the embryo metabolizes yolk steroids to regulate exposure. The 5β-reduction of steroids by the enzyme 5β-reductase (AKR1D1) has been identified as a pathway through which yolk progesterone, testosterone, and corticosterone are all metabolized early in avian development. We set out to characterize the mechanism through which AKR1D1 expression is regulated in chickens (Gallus gallus) during embryonic development. We found a synthetic and endogenous ligand (22R-hydroxycholesterol) for Liver X Receptor α (LXRα) induced AKR1D1 expression in the embryo and extraembryonic membranes on Day 2 of development. These results suggest that endogenous ligands of LXRα induce AKR1D1 expression and regulate the metabolism of yolk steroids during development.