Disruption of Tsc2 in oocytes leads to overactivation of the entire pool of primordial follicles

• DOI: 10.1093/molehr/gap092
• Publication Date: 2009-10-21T01:09:19Z
• Authors: D. Adhikari; G. Flohr; N. Gorre; Y. Shen; H. Yang; E. Lundin; Z. Lan; M. J. Gambello; K. Liu
• Keywords: TSC1; TSC2

To maintain the length of reproductive life in a woman, it is essential that most her ovarian primordial follicles are maintained quiescent state to provide continuous supply oocytes. However, our understanding molecular mechanisms control quiescence and activation still its infancy. In this study, we some genetic evidence show tumor suppressor tuberous sclerosis complex 2 (Tsc2), which negatively regulates mammalian target rapamycin 1 (mTORC1), functions oocytes dormancy follicles. mutant mice lacking Tsc2 gene oocytes, pool activated prematurely due elevated mTORC1 activity This results depletion early adulthood, causing premature failure (POF). Our suggest Tsc1–Tsc2 mediated suppression indispensable for maintenance follicles, thus preserving follicular pool, promotes activation. also indicate deregulation Tsc/mTOR signaling may cause pathological conditions ovary such as infertility POF.