FSH activates the PI3K/AKT pathway and thereby enhances granulosa cell differentiation in culture. To identify the physiological role of the PI3K pathway in vivo we disrupted the PI3K suppressor, Pten, in developing ovarian follicles. To selectively disrupt Pten expression in granulosa cells, Pten^fl/fl mice were mated with transgenic mice expressing CRE recombinase driven by Cyp19 promoter (Cyp19-Cre). The resultant Pten mutant mice were fertile, ovulated more oocytes and produced moderately more pups than control mice. These physiological differences in the Pten mutant mice were associated with hyper-activation of the PI3K/AKT pathway, decreased susceptibility to apoptosis, and increased proliferation of mutant granulosa cells. Strikingly, corpora lutea of the Pten mutant mice persisted longer than those of control mice. Although the follicular and luteal cell steroidogenesis in Pten^fl/fl;Cyp19-Cre mice was similar to controls, viable non-steroidogenic luteal cells escaped structural luteolysis. These findings provide the novel evidence that Pten impacts the survival/life-span of granulosa/luteal cells and that its loss not only results in the facilitated ovulation but also in the persistence of non-steroidogenic luteal structures in the adult mouse ovary.