Substantial evidence accumulated over six decades has established that estradiol exerts a dominant stimulatory influence on the production of progesterone by luteal tissue in pseudopregnant or pregnant rabbits, beginning approximately five days after ovulation. The direct steroidogenic action of estradiol on the luteal cell is mediated by the estrogen-receptor protein complex at the nuclear level. Major effects of estradiol lie distal to cholesterol ester and the formation of lipid droplets, and proximal to cholesterol availability for translocation into cytochrome P-450 cholesterol side-chain cleavage enzyme (P-450scc). Structure-function studies corroborate this as an estrogen-sensitive segment of the steroidogenic pathway in the rabbit corpus luteum. Estradiol increases the amount of precursor available for pregnenolone production in rabbit luteal mitochondria. Whether this is because of enhanced precursor storage in the mitochondria or because of effects on intramitochondrial movement of precursor, or both, is unclear. There is a void in knowledge between events at the nuclear level in response to the estrogen stimulus and known post-translational effects at the level of cellular and subcellular organelles. Studies to determine estrogen-sensitive transcriptional and translational events associated with steroidogenesis in the rabbit luteal cell model offer a novel perspective for an improved understanding of the regulatory processes governing steroidogenesis.