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SLC25A51 is a mammalian mitochondrial NAD~+ transporter

机译：SLC25A51是哺乳动物线粒体NAD〜+运输扣

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摘要

Mitochondria require nicotinamide adenine dinucleotide (NAD~(+)) to carry out the fundamental processes that fuel respiration and mediate cellular energy transduction. Mitochondrial NAD~(+)transporters have been identified in yeast and plants~(1,2), but their existence in mammals remains controversial~(3-5). Here we demonstrate that mammalian mitochondria can take up intact NAD~(+), and identify SLC25A51 (also known as MCART1)-an essential~(6,7)mitochondrial protein of previously unknown function-as a mammalian mitochondrial NAD~(+)transporter. Loss of SLC25A51 decreases mitochondrial-but not whole-cell-NAD~(+)content, impairs mitochondrial respiration, and blocks the uptake of NAD~(+)into isolated mitochondria. Conversely, overexpression of SLC25A51 or SLC25A52 (a nearly identical paralogue of SLC25A51) increases mitochondrial NAD~(+)levels and restores NAD~(+)uptake into yeast mitochondria lacking endogenous NAD~(+)transporters. Together, these findings identify SLC25A51 as a mammalian transporter capable of importing NAD~(+)into mitochondria.
机译：线粒体需要烟酰胺腺嘌呤二核苷酸（NAD〜（+））以进行燃料呼吸和介导细胞能量转导的根本过程。线粒体NAD〜（+）转运蛋白已在酵母和植物中鉴定〜（1,2），但它们在哺乳动物中的存在仍存在争议〜（3-5）。在这里，我们证明哺乳动物线粒体可以占用完整的NAD〜（+），并鉴定SLC25A51（也称为McART1）-an至必要的〜（6,7）线粒体蛋白质的先前未知的功能 - 作为哺乳动物线粒体NAD〜（+）运输车。 SLC25A51的丧失降低了线粒体 - 但不是全细胞 - NAD〜（+）含量，损害线粒体呼吸，并阻止NAD〜（+）的摄取到分离的线粒体中。相反，SLC25A51或SLC25A52的过度表达（SLC25A51的几乎相同的常例性）增加了线粒体NAD〜（+）水平并将NAD〜（+）摄取恢复到缺乏内源性NAD〜（+）转运蛋白的酵母线粒体中。这些发现一起鉴定了SLC25A51作为能够将NAD〜（+）导入线粒体的哺乳动物转运物。

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  • 来源
    《Nature》 |2020年第7836期|174-179|共6页
  • 作者

    Timothy S Luongo; Jared M Eller; Mu-Jie Lu; Marc Niere; Fabio Raith; Caroline Perry; Marc R Bornstein; Paul Oliphint; Lin Wang; Melanie R McReynolds; Marie E Migaud; Joshua D Rabinowitz; F Brad Johnson; Kai Johnsson; Mathias Ziegler; Xiaolu A Cambronne; Joseph A Baur;

  • 作者单位

    Department of Physiology and Institute for Diabetes Obesity and Metabolism Perelman School of Medicine University of Pennsylvania;

    Department of Molecular Biosciences University of Texas at Austin;

    Department of Molecular Biosciences University of Texas at Austin;

    Department of Biomedicine University of Bergen;

    Department of Chemical Biology Max Planck Institute for Medical Research|Faculty of Chemistry and Earth Sciences University of Heidelberg;

    Department of Physiology and Institute for Diabetes Obesity and Metabolism Perelman School of Medicine University of Pennsylvania;

    Department of Physiology and Institute for Diabetes Obesity and Metabolism Perelman School of Medicine University of Pennsylvania;

    Department of Molecular Biosciences University of Texas at Austin;

    Lewis-Sigler Institute for Integrative Genomics Department of Chemistry Princeton University;

    Lewis-Sigler Institute for Integrative Genomics Department of Chemistry Princeton University;

    Mitchell Cancer Institute University of South Alabama;

    Lewis-Sigler Institute for Integrative Genomics Department of Chemistry Princeton University;

    Department of Pathology and Laboratory Medicine Perlman School of Medicine University of Pennsylvania;

    Department of Chemical Biology Max Planck Institute for Medical Research|Institute of Chemical Sciences and Engineering École Polytechnique Fédérale de Lausanne (EPFL);

    Department of Biomedicine University of Bergen;

    Department of Molecular Biosciences University of Texas at Austin;

    Department of Physiology and Institute for Diabetes Obesity and Metabolism Perelman School of Medicine University of Pennsylvania;

  • 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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