mTOR (mammalian target of Rapamycin) is an important signaling pathway involved in several crucial ovarian functions including folliculogenesis and oocyte maturation. The circadian rhythm regulates multiple physiological processes and PER2 is one of the core circadian rhythm components. mTOR is regulated by the circadian clock and in turn, the rhythmic mTOR activities strengthen the clock function. Our current study aims to investigate a possible interconnection between the circadian clock and the mTORC1 signaling pathway in folliculogenesis and oocyte maturation. Here we demonstrate that the circadian system regulates mTORC1 signaling via Per2 dependent mechanism in the mouse ovary. To investigate the effect of constant light on ovarian and oocyte morphology, animals were housed 12:12 h L:D group in standard lightening conditions and the 12:12 h L:L group in constant light for one week. Food intake and body weight changes were measured. Ovarian morphology, follicle counting, and oocyte aging were evaluated. Afterward, western blot for mTOR, p-mTOR, p70S6K, p-p70S6K, PER2, and Caspase-3 protein levels was performed. The study demonstrated that circadian rhythm disruption caused an alteration in their food intake and decrease in primordial follicle numbers and an increase in the number of atretic follicles. It caused an increase in oxidative stress and a decrease in ZP3 expression in oocytes. Decreased protein levels of mTOR, p-mTOR, p70S6K, and PER2 were shown. The results showed that the circadian clock regulates mTORC1 through PER2 dependent mechanism and that decreased mTORC1 activity can contribute to premature aging of mouse ovary. In conclusion, these results suggest that the circadian clock may control ovarian aging by regulating mTOR signaling pathway through Per2 expression.

mTOR（雷帕霉素的哺乳动物靶标）是一条重要的信号通路，涉及卵泡发生和卵母细胞成熟等多种重要的卵巢功能。昼夜节律调节多种生理过程，PER2是昼夜节律的核心组成部分之一。mTOR 受生物钟调节，有节律的 mTOR 活动反过来又增强了生物钟功能。我们目前的研究旨在探讨生物钟与 mTORC1 信号通路在卵泡发生和卵母细胞成熟中可能存在的相互联系。在这里，我们证明昼夜节律系统通过小鼠卵巢中的 Per2 依赖性机制调节 mTORC1 信号传导。为了研究恒定光照对卵巢和卵母细胞形态的影响，将动物饲养在标准光照条件下的 12:12 h L:D 组和 12:12 h L:D 组中。12小时L:L组在恒定光照下持续一周。测量食物摄入量和体重变化。评估卵巢形态、卵泡计数和卵母细胞老化。随后，对 mTOR、p-mTOR、p70S6K、p-p70S6K、PER2 和 Caspase-3 蛋白水平进行蛋白质印迹。研究表明，昼夜节律紊乱导致食物摄入量发生变化，原始卵泡数量减少，闭锁卵泡数量增加。它导致卵母细胞氧化应激增加和 ZP3 表达减少。mTOR、p-mTOR、p70S6K 和 PER2 的蛋白质水平降低。结果表明，生物钟通过PER2依赖性机制调节mTORC1，mTORC1活性降低可导致小鼠卵巢过早衰老。综上所述，