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Post-translational regulation of mTOR complex 1 in hypoxia and reoxygenation

机译：低氧和复氧条件下mTOR复合体1的翻译后调节

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The mechanistic target of rapamycin complex 1 (mTORC1) is a key regulator of cell growth and proliferation in response to various upstream signals. Hypoxia has been shown to exert a strong inhibitory effect on mTORC1 activity. Various mechanisms involving gene transcription have been proposed to mediate the effect of hypoxia on mTORC1 activity. Here we show that oxygen concentrations regulate mTORC1 activity in a highly dynamic manner. The rapid response of mTORC1 to changes in oxygen concentrations was not mediated by the HIF transcription factor or its transcriptional targets, REDD1 and BNIP3. Interestingly, we observed that the rapid response of mTORC1 activity to changes in oxygen concentrations is independent of transcription and new protein synthesis. This suggests a post-translational regulation mTORC1 activity in hypoxia and reoxygenation. We also provide evidence that hypoxia does not regulate mTORC1 via the TSC1/2 or Ragulator pathways but directly at the level of mTORC1. In conclusion, our results suggest that mTORC1 can respond rapidly to changes in oxygen concentrations via a post-translational mechanism that may involve a heme containing protein.
机译：雷帕霉素复合物1（mTORC1）的机械目标是响应各种上游信号的细胞生长和增殖的关键调节剂。缺氧已显示出对mTORC1活性具有强大的抑制作用。已经提出了多种涉及基因转录的机制来介导缺氧对mTORC1活性的影响。在这里，我们显示氧浓度以高度动态的方式调节mTORC1的活性。 HIF转录因子或其转录靶REDD1和BNIP3并未介导mTORC1对氧浓度变化的快速反应。有趣的是，我们观察到mTORC1活性对氧浓度变化的快速响应与转录和新蛋白合成无关。这表明在缺氧和复氧的翻译后调节mTORC1活性。我们还提供证据表明缺氧并不通过TSC1 / 2或Ragulator途径调节mTORC1，而是直接在mTORC1的水平上调节。总之，我们的结果表明mTORC1可以通过翻译后机制快速响应氧浓度的变化，该机制可能涉及含有血红素的蛋白质。

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