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SLC25A51 is a mammalian mitochondrial NAD+ transporter.
Metadata
Journalnature42.778Date
2020 Sep 09
21 days ago
Type
Journal Article
Volume
2020-Sep-09 / :
Author
Luongo TS 1, Eller JM 2, Lu MJ 2, Niere M 3, Raith F 4, 5, Perry C 1, Bornstein MR 1, Oliphint P 2, Wang L 6, McReynolds MR 6, Migaud ME 7, Rabinowitz JD 6, Johnson FB 8, Johnsson K 4, 9, Ziegler M 3, Cambronne XA 10, Baur JA 11
Affiliation
  • 2. Department of Molecular Biosciences, University of Texas at Austin, Austin, Texas, 78712, USA.
  • 3. Department of Biomedicine, University of Bergen, 5009, Bergen, Norway.
  • 4. Department of Chemical Biology, Max Planck Institute for Medical Research, 69120, Heidelberg, Germany.
  • 5. Faculty of Chemistry and Earth Sciences, University of Heidelberg, 69120, Heidelberg, Germany.
  • 6. Lewis-Sigler Institute for Integrative Genomics, Department of Chemistry, Princeton University, Princeton, NJ, USA.
  • 7. Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
  • 8. Department of Pathology and Laboratory Medicine, Perlman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, U.S.A.
  • 9. Institute of Chemical Sciences and Engineering, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
  • 10. Department of Molecular Biosciences, University of Texas at Austin, Austin, Texas, 78712, USA. [email protected]
  • 11. Department of Physiology and Institute for Diabetes, Obesity, and Metabolism Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, U.S.A.. [email protected]
Doi
PMIDMESH
Abstract
Mitochondria require nicotinamide adenine dinucleotide (NAD+) in order to carry out the fundamental processes that fuel respiration and mediate cellular energy transduction. Mitochondrial NAD+ transporters have been identified in yeast and plants1,2 but their very existence is controversial in mammals3-5. Here we demonstrate that mammalian mitochondria are capable of taking up intact NAD+ and identify SLC25A51 (an essential6,7 mitochondrial protein of previously unknown function, also known as MCART1) 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 a nearly identical paralog, SLC25A52, increases mitochondrial NAD+ levels and restores NAD+ uptake into yeast mitochondria lacking endogenous NAD+ transporters. Together, these findings identify SLC25A51 as the first transporter capable of importing NAD+ into mammalian mitochondria.
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