Epistasis-driven identification of SLC25A51 as a regulator of human mitochondrial NAD import.

Détails

Ressource 1Télécharger: 41467_2020_Article_19871.pdf (1362.81 [Ko])
Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_75C6C477E13D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Epistasis-driven identification of SLC25A51 as a regulator of human mitochondrial NAD import.
Périodique
Nature communications
Auteur⸱e⸱s
Girardi E., Agrimi G., Goldmann U., Fiume G., Lindinger S., Sedlyarov V., Srndic I., Gürtl B., Agerer B., Kartnig F., Scarcia P., Di Noia M.A., Liñeiro E., Rebsamen M., Wiedmer T., Bergthaler A., Palmieri L., Superti-Furga G.
ISSN
2041-1723 (Electronic)
ISSN-L
2041-1723
Statut éditorial
Publié
Date de publication
01/12/2020
Peer-reviewed
Oui
Volume
11
Numéro
1
Pages
6145
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Résumé
About a thousand genes in the human genome encode for membrane transporters. Among these, several solute carrier proteins (SLCs), representing the largest group of transporters, are still orphan and lack functional characterization. We reasoned that assessing genetic interactions among SLCs may be an efficient way to obtain functional information allowing their deorphanization. Here we describe a network of strong genetic interactions indicating a contribution to mitochondrial respiration and redox metabolism for SLC25A51/MCART1, an uncharacterized member of the SLC25 family of transporters. Through a combination of metabolomics, genomics and genetics approaches, we demonstrate a role for SLC25A51 as enabler of mitochondrial import of NAD, showcasing the potential of genetic interaction-driven functional gene deorphanization.
Mots-clé
Biological Transport, Epistasis, Genetic, Humans, Mitochondria/genetics, Mitochondria/metabolism, NAD/metabolism, Oxidation-Reduction, Uncoupling Protein 1/genetics, Uncoupling Protein 1/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
07/02/2022 10:01
Dernière modification de la notice
05/04/2023 12:04
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