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SLC25A51 is a mammalian mitochondrial NAD+ transporter

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Raith,  Fabio
Cellular Biophysics, Max Planck Institute for Medical Research, Max Planck Society;

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Johnsson,  Kai
Chemical Biology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Luongo, T. S., Eller, J. M., Lu, M.-J., Niere, M., Raith, F., Perry, C., et al. (2020). SLC25A51 is a mammalian mitochondrial NAD+ transporter. Nature, 588, 174-179. doi:10.1038/s41586-020-2741-7.


Cite as: http://hdl.handle.net/21.11116/0000-0007-6FEB-5
Abstract
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 plants1,2, but their existence in mammals remains controversial3,4,5. Here we demonstrate that mammalian mitochondria can take up intact NAD+, and identify SLC25A51 (also known as MCART1)—an essential6,7 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.