Rev1 contributes to proper mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1 alpha axis

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Rev1 contributes to proper mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1 alpha axis. / Fakouri, Nima Borhan; Durhuus, Jon Ambaek; Regnell, Christine Elisabeth; Angleys, Maria; Desler, Claus; Hasan-Olive, Mahdi; Martin-Pardillos, Ana; Tsaalbi-Shtylik, Anastasia; Thomsen, Kirsten; Lauritzen, Martin; Bohr, Vilhelm A.; de Wind, Niels; Bergersen, Linda Hildegard; Rasmussen, Lene Juel.

In: Scientific Reports, Vol. 7, 12480, 2017.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Fakouri, NB, Durhuus, JA, Regnell, CE, Angleys, M, Desler, C, Hasan-Olive, M, Martin-Pardillos, A, Tsaalbi-Shtylik, A, Thomsen, K, Lauritzen, M, Bohr, VA, de Wind, N, Bergersen, LH & Rasmussen, LJ 2017, 'Rev1 contributes to proper mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1 alpha axis', Scientific Reports, vol. 7, 12480. https://doi.org/10.1038/s41598-017-12662-3

APA

Fakouri, N. B., Durhuus, J. A., Regnell, C. E., Angleys, M., Desler, C., Hasan-Olive, M., ... Rasmussen, L. J. (2017). Rev1 contributes to proper mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1 alpha axis. Scientific Reports, 7, [12480]. https://doi.org/10.1038/s41598-017-12662-3

Vancouver

Fakouri NB, Durhuus JA, Regnell CE, Angleys M, Desler C, Hasan-Olive M et al. Rev1 contributes to proper mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1 alpha axis. Scientific Reports. 2017;7. 12480. https://doi.org/10.1038/s41598-017-12662-3

Author

Fakouri, Nima Borhan ; Durhuus, Jon Ambaek ; Regnell, Christine Elisabeth ; Angleys, Maria ; Desler, Claus ; Hasan-Olive, Mahdi ; Martin-Pardillos, Ana ; Tsaalbi-Shtylik, Anastasia ; Thomsen, Kirsten ; Lauritzen, Martin ; Bohr, Vilhelm A. ; de Wind, Niels ; Bergersen, Linda Hildegard ; Rasmussen, Lene Juel. / Rev1 contributes to proper mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1 alpha axis. In: Scientific Reports. 2017 ; Vol. 7.

Bibtex

@article{58d7262d0b6248d89ec15db3164f9578,
title = "Rev1 contributes to proper mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1 alpha axis",
abstract = "Nucleic acids, which constitute the genetic material of all organisms, are continuously exposed to endogenous and exogenous damaging agents, representing a significant challenge to genome stability and genome integrity over the life of a cell or organism. Unrepaired DNA lesions, such as single- and double-stranded DNA breaks (SSBs and DSBs), and single-stranded gaps can block progression of the DNA replication fork, causing replicative stress and/or cell cycle arrest. However, translesion synthesis (TLS) DNA polymerases, such as Rev1, have the ability to bypass some DNA lesions, which can circumvent the process leading to replication fork arrest and minimize replicative stress. Here, we show that Rev1-deficiency in mouse embryo fibroblasts or mouse liver tissue is associated with replicative stress and mitochondrial dysfunction. In addition, Rev1-deficiency is associated with high poly(ADP) ribose polymerase 1 (PARP1) activity, low endogenous NAD+, low expression of SIRT1 and PGC1α and low adenosine monophosphate (AMP)-activated kinase (AMPK) activity. We conclude that replication stress via Rev1-deficiency contributes to metabolic stress caused by compromized mitochondrial function via the PARP-NAD+-SIRT1-PGC1α axis.",
author = "Fakouri, {Nima Borhan} and Durhuus, {Jon Ambaek} and Regnell, {Christine Elisabeth} and Maria Angleys and Claus Desler and Mahdi Hasan-Olive and Ana Martin-Pardillos and Anastasia Tsaalbi-Shtylik and Kirsten Thomsen and Martin Lauritzen and Bohr, {Vilhelm A.} and {de Wind}, Niels and Bergersen, {Linda Hildegard} and Rasmussen, {Lene Juel}",
note = "Author Correction: Rev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1α axis DOI: 10.1038/s41598-018-20586-9",
year = "2017",
doi = "10.1038/s41598-017-12662-3",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Rev1 contributes to proper mitochondrial function via the PARP-NAD(+)-SIRT1-PGC1 alpha axis

AU - Fakouri, Nima Borhan

AU - Durhuus, Jon Ambaek

AU - Regnell, Christine Elisabeth

AU - Angleys, Maria

AU - Desler, Claus

AU - Hasan-Olive, Mahdi

AU - Martin-Pardillos, Ana

AU - Tsaalbi-Shtylik, Anastasia

AU - Thomsen, Kirsten

AU - Lauritzen, Martin

AU - Bohr, Vilhelm A.

AU - de Wind, Niels

AU - Bergersen, Linda Hildegard

AU - Rasmussen, Lene Juel

N1 - Author Correction: Rev1 contributes to proper mitochondrial function via the PARP-NAD+-SIRT1-PGC1α axis DOI: 10.1038/s41598-018-20586-9

PY - 2017

Y1 - 2017

N2 - Nucleic acids, which constitute the genetic material of all organisms, are continuously exposed to endogenous and exogenous damaging agents, representing a significant challenge to genome stability and genome integrity over the life of a cell or organism. Unrepaired DNA lesions, such as single- and double-stranded DNA breaks (SSBs and DSBs), and single-stranded gaps can block progression of the DNA replication fork, causing replicative stress and/or cell cycle arrest. However, translesion synthesis (TLS) DNA polymerases, such as Rev1, have the ability to bypass some DNA lesions, which can circumvent the process leading to replication fork arrest and minimize replicative stress. Here, we show that Rev1-deficiency in mouse embryo fibroblasts or mouse liver tissue is associated with replicative stress and mitochondrial dysfunction. In addition, Rev1-deficiency is associated with high poly(ADP) ribose polymerase 1 (PARP1) activity, low endogenous NAD+, low expression of SIRT1 and PGC1α and low adenosine monophosphate (AMP)-activated kinase (AMPK) activity. We conclude that replication stress via Rev1-deficiency contributes to metabolic stress caused by compromized mitochondrial function via the PARP-NAD+-SIRT1-PGC1α axis.

AB - Nucleic acids, which constitute the genetic material of all organisms, are continuously exposed to endogenous and exogenous damaging agents, representing a significant challenge to genome stability and genome integrity over the life of a cell or organism. Unrepaired DNA lesions, such as single- and double-stranded DNA breaks (SSBs and DSBs), and single-stranded gaps can block progression of the DNA replication fork, causing replicative stress and/or cell cycle arrest. However, translesion synthesis (TLS) DNA polymerases, such as Rev1, have the ability to bypass some DNA lesions, which can circumvent the process leading to replication fork arrest and minimize replicative stress. Here, we show that Rev1-deficiency in mouse embryo fibroblasts or mouse liver tissue is associated with replicative stress and mitochondrial dysfunction. In addition, Rev1-deficiency is associated with high poly(ADP) ribose polymerase 1 (PARP1) activity, low endogenous NAD+, low expression of SIRT1 and PGC1α and low adenosine monophosphate (AMP)-activated kinase (AMPK) activity. We conclude that replication stress via Rev1-deficiency contributes to metabolic stress caused by compromized mitochondrial function via the PARP-NAD+-SIRT1-PGC1α axis.

UR - https://doi.org/10.1038/s41598-018-20586-9

U2 - 10.1038/s41598-017-12662-3

DO - 10.1038/s41598-017-12662-3

M3 - Journal article

C2 - 28970491

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 12480

ER -

ID: 184769933