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Identification of an ATP - sensitive potassium channel in mitochondria

机译：鉴定线粒体中ATP敏感钾通道的鉴定

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摘要

Mitochondria provide chemical energy for endoergonic reactions in the form of ATP, and their activity must meet cellular energy requirements, but the mechanisms that link organelle performance to ATP levels are poorly understood. Here we confirm the existence of a protein complex localized in mitochondria that mediates ATP-dependent potassium currents (that is, mitoK(ATP)). We show that-similar to their plasma membrane counterparts-mitoK(ATP) channels are composed of pore-forming and ATP-binding subunits, which we term MITOK and MITOSUR, respectively. In vitro reconstitution of MITOK together with MITOSUR recapitulates the main properties of mitoK(ATP). Overexpression of MITOK triggers marked organelle swelling, whereas the genetic ablation of this subunit causes instability in the mitochondrial membrane potential, widening of the intracristal space and decreased oxidative phosphorylation. In a mouse model, the loss of MITOK suppresses the cardioprotection that is elicited by pharmacological preconditioning induced by diazoxide. Our results indicate that mitoK(ATP) channels respond to the cellular energetic status by regulating organelle volume and function, and thereby have a key role in mitochondrial physiology and potential effects on several pathological processes.
机译：线粒体为ATP的形式提供了用于内沸剂反应的化学能，它们的活性必须满足细胞能量要求，但将细胞器性能与ATP水平的机制很难以理解。在这里，我们确认存在于介导ATP依赖性钾电流的线粒体中局部化的蛋白质复合物（即，MITOK（ATP））。我们展示 - 类似于它们的血浆膜对应 - MITOK（ATP）通道分别由我们术语MINOK和MITOSUR学期的孔形成和ATP结合亚基组成。与MITOOUR一起进行米托克的体外重建概述了MINOK（ATP）的主要性质。 MINOK的过度表达触发标记有细胞器肿胀，而该亚基的遗传烧蚀导致线粒体膜电位的不稳定性，颅内空间的扩大并降低氧化磷酸化。在小鼠模型中，MINOOK的丧失抑制了通过二氧氮酰胺诱导的药理学预处理引发的心脏保护。我们的结果表明，MITOK（ATP）通道通过调节细胞器体积和功能来响应细胞能量状态，从而对线粒体生理学和对几种病理过程的潜在影响具有关键作用。

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  • 来源
    《Nature》 |2019年第7771期|609-613|共5页
  • 作者

    Paggio Angela; Checchetto Vanessa; Campo Antonio; Menabo Roberta; Di Marco Giulia; Di Lisa Fabio; Szabo Ildiko; Rizzuto Rosario; De Stefani Diego;

  • 作者单位

    Univ Padua Dept Biomed Sci Padua Italy;

    Univ Padua Dept Biol Padua Italy;

    Univ Padua Dept Biomed Sci Padua Italy;

    CNR Inst Neurosci Padua Italy;

    Univ Padua Dept Biomed Sci Padua Italy;

    Univ Padua Dept Biomed Sci Padua Italy|CNR Inst Neurosci Padua Italy;

    Univ Padua Dept Biol Padua Italy|CNR Inst Neurosci Padua Italy;

    Univ Padua Dept Biomed Sci Padua Italy;

    Univ Padua Dept Biomed Sci Padua Italy;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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  • 正文语种 eng
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