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首页> 外文期刊>Cell metabolism >Let-7 coordinately suppresses components of the amino acid sensing pathway to repress mTORC1 and induce autophagy
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Let-7 coordinately suppresses components of the amino acid sensing pathway to repress mTORC1 and induce autophagy

机译：Let-7协同抑制氨基酸感应途径的成分，从而抑制mTORC1并诱导自噬

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Macroautophagy (hereafter autophagy) is the major pathway by which macromolecules and organelles are degraded. Autophagy is regulated by the mTOR signaling pathway - the focal point for integration of metabolic information, with mTORC1 playing a central role in balancing biosynthesis and catabolism. Of the various inputs to mTORC1, the amino acid sensing pathway is among the most potent. Based upon transcriptome analysis of neurons subjected to nutrient deprivation, we identified let-7 microRNA as capable of promoting neuronal autophagy. We found that let-7 activates autophagy by coordinately downregulating the amino acid sensing pathway to prevent mTORC1 activation. Let-7 induced autophagy in the brain to eliminate protein aggregates, establishing its physiological relevance for in vivo autophagy modulation. Moreover, peripheral delivery of let-7 anti-miR repressed autophagy in muscle and white fat, suggesting that let-7 autophagy regulation extends beyond CNS. Hence, let-7 plays a central role in nutrient homeostasis and proteostasis regulation in higher organisms.
机译：大分子自噬（以下称自噬）是降解大分子和细胞器的主要途径。自噬受mTOR信号通路（代谢信息整合的焦点）调控，而mTORC1在平衡生物合成和分解代谢中起着核心作用。在mTORC1的各种输入中，氨基酸感应途径是最有效的途径之一。根据对营养缺乏的神经元的转录组分析，我们确定let-7 microRNA能够促进神经元自噬。我们发现let-7通过协调性下调氨基酸传感途径来阻止mTORC1激活，从而激活自噬。 Let-7在大脑中诱导自噬以消除蛋白质聚集体，从而确立了其与体内自噬调节的生理相关性。此外，let-7抗miR的外周递送抑制了肌肉和白色脂肪中的自噬，这表明let-7自噬的调控范围超出了中枢神经系统。因此，let-7在高等生物体的营养稳态和蛋白稳态调节中起着核心作用。

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