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

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 a...

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Published inNature communications Vol. 11; no. 1; pp. 6145 - 9
Main Authors Girardi, Enrico, Agrimi, Gennaro, Goldmann, Ulrich, Fiume, Giuseppe, Lindinger, Sabrina, Sedlyarov, Vitaly, Srndic, Ismet, Gürtl, Bettina, Agerer, Benedikt, Kartnig, Felix, Scarcia, Pasquale, Di Noia, Maria Antonietta, Liñeiro, Eva, Rebsamen, Manuele, Wiedmer, Tabea, Bergthaler, Andreas, Palmieri, Luigi, Superti-Furga, Giulio
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.12.2020
Nature Publishing Group
Nature Portfolio
Subjects
13/106
13/44
45
49
631/443/319
631/80/642/333
631/80/642/333/1465
Biological Transport
CRISPR
Epistasis
Epistasis, Genetic
Genes
Genetics
Genomics
Homology
Humanities and Social Sciences
Humans
Imports
Localization
Metabolism
Metabolomics
Mitochondria
Mitochondria - genetics
Mitochondria - metabolism
multidisciplinary
NAD
NAD - metabolism
Oxidation-Reduction
Science
Science (multidisciplinary)
Uncoupling Protein 1 - genetics
Uncoupling Protein 1 - metabolism
Yeast
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Abstract 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. Maintenance of a mitochondrial NAD+ pool is critical for cellular life, yet the existence and identity of the transporter responsible for mitochondrial NAD+ uptake was unknown until recently. Here, the authors use genomic, genetic, and metabolomic approaches to demonstrate that SLC25A51 controls NAD+ mitochondrial levels and is the functional homolog of the yeast mitochondrial NAD+ transporter.
AbstractList 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.
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. Maintenance of a mitochondrial NAD+ pool is critical for cellular life, yet the existence and identity of the transporter responsible for mitochondrial NAD+ uptake was unknown until recently. Here, the authors use genomic, genetic, and metabolomic approaches to demonstrate that SLC25A51 controls NAD+ mitochondrial levels and is the functional homolog of the yeast mitochondrial NAD+ transporter.
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.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.
Maintenance of a mitochondrial NAD+ pool is critical for cellular life, yet the existence and identity of the transporter responsible for mitochondrial NAD+ uptake was unknown until recently. Here, the authors use genomic, genetic, and metabolomic approaches to demonstrate that SLC25A51 controls NAD+ mitochondrial levels and is the functional homolog of the yeast mitochondrial NAD+ transporter.
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.Maintenance of a mitochondrial NAD+ pool is critical for cellular life, yet the existence and identity of the transporter responsible for mitochondrial NAD+ uptake was unknown until recently. Here, the authors use genomic, genetic, and metabolomic approaches to demonstrate that SLC25A51 controls NAD+ mitochondrial levels and is the functional homolog of the yeast mitochondrial NAD+ transporter.
ArticleNumber 6145
Author Sedlyarov, Vitaly
Agerer, Benedikt
Bergthaler, Andreas
Scarcia, Pasquale
Di Noia, Maria Antonietta
Superti-Furga, Giulio
Rebsamen, Manuele
Fiume, Giuseppe
Liñeiro, Eva
Agrimi, Gennaro
Srndic, Ismet
Girardi, Enrico
Lindinger, Sabrina
Kartnig, Felix
Wiedmer, Tabea
Palmieri, Luigi
Goldmann, Ulrich
Gürtl, Bettina
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/33262325$$D View this record in MEDLINE/PubMed
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Snippet About a thousand genes in the human genome encode for membrane transporters. Among these, several solute carrier proteins (SLCs), representing the largest...
Maintenance of a mitochondrial NAD+ pool is critical for cellular life, yet the existence and identity of the transporter responsible for mitochondrial NAD+...
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SubjectTerms 13/106
13/44
45
49
631/443/319
631/80/642/333
631/80/642/333/1465
Biological Transport
CRISPR
Epistasis
Epistasis, Genetic
Genes
Genetics
Genomics
Homology
Humanities and Social Sciences
Humans
Imports
Localization
Metabolism
Metabolomics
Mitochondria
Mitochondria - genetics
Mitochondria - metabolism
multidisciplinary
NAD
NAD - metabolism
Oxidation-Reduction
Science
Science (multidisciplinary)
Uncoupling Protein 1 - genetics
Uncoupling Protein 1 - metabolism
Yeast
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Title Epistasis-driven identification of SLC25A51 as a regulator of human mitochondrial NAD import
URI https://link.springer.com/article/10.1038/s41467-020-19871-x
https://www.ncbi.nlm.nih.gov/pubmed/33262325
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https://pubmed.ncbi.nlm.nih.gov/PMC7708531
https://doaj.org/article/e8ac6a683e1a429f8d643e2061a12835
Volume 11
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