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The Circadian Protein Period2 Suppresses mTORC1 Activity via Recruiting Tsc1 to mTORC1 Complex.
Cell Metabolism ( IF 27.7 ) Pub Date : 2018-12-06 , DOI: 10.1016/j.cmet.2018.11.006 Rong Wu 1 , Fabin Dang 1 , Peng Li 1 , Pengfei Wang 1 , Qian Xu 2 , Zhengshuai Liu 1 , Yu Li 1 , Yuting Wu 1 , Yaqiong Chen 3 , Yi Liu 3
Cell Metabolism ( IF 27.7 ) Pub Date : 2018-12-06 , DOI: 10.1016/j.cmet.2018.11.006 Rong Wu 1 , Fabin Dang 1 , Peng Li 1 , Pengfei Wang 1 , Qian Xu 2 , Zhengshuai Liu 1 , Yu Li 1 , Yuting Wu 1 , Yaqiong Chen 3 , Yi Liu 3
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Although emerging evidence indicates an important role of the circadian clock in modulating the diurnal oscillation of mammalian target of rapamycin complex 1 (mTORC1) signaling, the underlying molecular mechanism remains elusive. Here we show that Period2 (Per2), a core clock protein, functions as a scaffold protein to tether tuberous sclerosis complex 1 (Tsc1), Raptor, and mTOR together to specifically suppress the activity of mTORC1 complex. Due to the loss of its inhibition of mTORC1, Per2 deficiency significantly enhances protein synthesis and cell proliferation but reduces autophagy. Furthermore, we find that the glucagon-Creb/Crtc2 signaling cascade induces Per2 expression, which mediates the suppression of mTORC1 in mouse liver during fasting. Our study not only uncovers a novel role of Per2 in regulating the mTORC1 pathway, but also sheds new light on the mechanism of fasting inhibition on mTORC1 in the liver.
中文翻译：
昼夜节律蛋白Period2通过将Tsc1招募至mTORC1复合体来抑制mTORC1活性。
尽管新出现的证据表明昼夜节律在调节雷帕霉素复合物1（mTORC1）信号转导哺乳动物靶标的昼夜振荡中起着重要作用，但潜在的分子机制仍然难以捉摸。在这里我们显示，Period2（Per2），一种核心时钟蛋白，起着束缚结节性硬化症复合物1（Tsc1），Raptor和mTOR的支架蛋白的作用，以特异性抑制mTORC1复合物的活性。由于失去了对mTORC1的抑制，Per2缺乏症显着增强了蛋白质合成和细胞增殖，但降低了自噬。此外，我们发现胰高血糖素-Creb / Crtc2信号级联反应诱导Per2表达，其在禁食期间介导小鼠肝脏中mTORC1的抑制。我们的研究不仅揭示了Per2在调节mTORC1途径中的新作用，
更新日期：2018-12-07
中文翻译：
昼夜节律蛋白Period2通过将Tsc1招募至mTORC1复合体来抑制mTORC1活性。
尽管新出现的证据表明昼夜节律在调节雷帕霉素复合物1（mTORC1）信号转导哺乳动物靶标的昼夜振荡中起着重要作用，但潜在的分子机制仍然难以捉摸。在这里我们显示，Period2（Per2），一种核心时钟蛋白，起着束缚结节性硬化症复合物1（Tsc1），Raptor和mTOR的支架蛋白的作用，以特异性抑制mTORC1复合物的活性。由于失去了对mTORC1的抑制，Per2缺乏症显着增强了蛋白质合成和细胞增殖，但降低了自噬。此外，我们发现胰高血糖素-Creb / Crtc2信号级联反应诱导Per2表达，其在禁食期间介导小鼠肝脏中mTORC1的抑制。我们的研究不仅揭示了Per2在调节mTORC1途径中的新作用，
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