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Tuberous sclerosis complex 1 ( Tsc1 ) is a tumor suppressor negatively regulating mammalian target of rapamycin complex 1 (mTORC1). It is reported that mice lacking  Tsc1  gene in oocytes show depletion of primordial follicles, resulting in premature ovarian failure and subsequent infertility. A recent study indicated that deletion of  Tsc1  in somatic cells of the reproductive tract caused infertility of female mice. However, it is not known whether specific disruption of  Tsc1  in granulosa cells influences the reproductive activity of female mice. To clarify this problem, we mated  Tsc1 flox/flox   mice with transgenic mice strain expressing cyp19-cre which exclusively expresses in granulosa cells of the ovary. Our results demonstrated that  Tsc1 flox/flox  ;  cyp19-cre  mutant mice were fertile, ovulating more oocytes and giving birth to more pups than control  Tsc1 flox/flox   mice. Progressive accumulation of corpora lutea occurred in the  Tsc1 flox/flox  ;  cyp19-cre  mutant mice with advanced age. These phenotypes could be explained by the elevated activity of mTORC1, as indicated by increased phosphorylation of rpS6, a substrate of S6 in the  Tsc1 flox/flox  ;  cyp19-cre  mutant granulosa cells. In addition, rapamycin, a specific mTORC1 inhibitor, effectively rescued the phenotype caused by increased mTORC1 activity in the  Tsc1 cko   ovaries. Our data suggest that conditional knockout of Tsc1 in granulosa cells promotes reproductive activity in mice.

Specific Disruption of Tsc1 in Ovarian Granulosa Cells Promotes Ovulation and Causes Progressive Accumulation of Corpora Lutea