The purpose of this investigation was to determine whether the timing of ovulation induction during the follicular phase is a determinant of consequent luteal function. Ewes were treated on day 14 of the estrous cycle with PGF2alpha to synchronize luteal regression and 12 or 36 h later with an ovulatory dose of GnRH. Luteal phase serum progesterone concentrations of normal magnitude were characteristic of animals elicited to ovulate by GnRH injection 36 h after PGF2alpha treatment. Follicles stimulated at 12 h of the induced follicular phase formed subfunctional corpora lutea that were deficient in large steroidogenic cells. Endometrial gland development was attenuated in ewes exhibiting luteal insufficiency. The pathophysiology of the luteal defect was associated with a retrospective lack of granulosal cells in preovulatory follicles not adequately primed by estradiol. Preovulatory LH surges were not affected by the time of GnRH treatment. Corpus luteum rescue indicative of maternal recognition of pregnancy occurred in inseminated ewes that were injected with GnRH 36 h after PGF2alpha. Gonadotropic stimulation 12 h after PGF2alpha typically resulted in gestational failure; a marginal improvement in the pregnancy rate was attained by progesterone supplementation. We suggest that premature induction of ovulation compromises the estrogen-mediated succession of granulosal cell proliferative events that necessitate the formation of a fully competent corpus luteum.