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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Nutrient starvation elicits an acute autophagic response mediated by Ulk1 dephosphorylation and its subsequent dissociation from AMPK
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Nutrient starvation elicits an acute autophagic response mediated by Ulk1 dephosphorylation and its subsequent dissociation from AMPK

机译：营养饥饿引发由Ulk1脱磷酸作用及其随后与AMPK分离介导的急性自噬反应

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摘要

Macroautophagy (herein referred to as autophagy) is an evolutionarily conserved self-digestive process cells adapt to starvation and other stress responses. Upon starvation, autophagy is induced, providing cells with needed nutrient supplies. We report here that Unc-51-like kinase 1 (Ulk1), a key initiator for mammalian autophagy, undergoes dramatic dephosphorylation upon starvation, particularly at serine 638 and serine 758. Phosphorylations of Ulk1 are mediated by mammalian target-of-rapamycin (mTOR) kinase and adenosine monophosphate activated protein kinase (AMPK). AMPK interacts with Ulk1 in a nutrient-dependent manner. Proper phosphorylations on Ulk1 are crucial for Ulk1/AMPK association, as a single serine-to-alanine mutation (S758A) at Ulk1 impairs this interaction. Compared to the wild-type ULK1, this Ulk1-S758A mutant initiates starvation-induced autophagy faster at an early time point, but does not alter the maximum capacity of autophagy when starvation prolongs. This study therefore revealed previously unnoticed acute autophagy response to environmental changes.
机译：巨自噬（在本文中称为自噬）是进化上保守的自消化过程细胞，其适应饥饿和其他应激反应。饥饿时会诱导自噬，为细胞提供所需的营养物质。我们在这里报告，Unc-51样激酶1（Ulk1），哺乳动物自噬的关键启动子，在饥饿时，尤其是在丝氨酸638和丝氨酸758处经历剧烈的去磷酸化。Ulk1的磷酸化是由哺乳动物雷帕霉素靶标（mTOR）介导的激酶和单磷酸腺苷活化蛋白激酶（AMPK）。 AMPK以营养依赖性方式与Ulk1相互作用。 Ulk1上正确的磷酸化对于Ulk1 / AMPK关联至关重要，因为Ulk1上的单个丝氨酸到丙氨酸突变（S758A）会削弱这种相互作用。与野生型ULK1相比，该Ulk1-S758A突变体在较早的时间点更快地启动了饥饿诱导的自噬，但是当饥饿延长时，它不会改变自噬的最大能力。因此，这项研究揭示了以前对环境变化未注意到的急性自噬反应。

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  • 作者

    Libin Shang; She Chen; Fenghe Du; Shen Li; Liping Zhao; Xiaodong Wang;

  • 作者单位

    Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390;

    National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China;

    Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390;

    National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China;

    Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390,National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China;

    Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390,National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    calcium; lc3; atg13; silac; pi3k;

    机译：钙;lc3;atg13;silac;pi3k;

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