Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair. / Akbari, Mansour; Keijzers, Guido; Maynard, Scott; Scheibye-Knudsen, Morten; Madsen, Claus Desler; Hickson, Ian D; Bohr, Vilhelm A.

In: DNA Repair, Vol. 16, 04.2014, p. 44-53.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Akbari, M, Keijzers, G, Maynard, S, Scheibye-Knudsen, M, Madsen, CD, Hickson, ID & Bohr, VA 2014, 'Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair', DNA Repair, vol. 16, pp. 44-53. https://doi.org/10.1016/j.dnarep.2014.01.015

APA

Akbari, M., Keijzers, G., Maynard, S., Scheibye-Knudsen, M., Madsen, C. D., Hickson, I. D., & Bohr, V. A. (2014). Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair. DNA Repair, 16, 44-53. https://doi.org/10.1016/j.dnarep.2014.01.015

Vancouver

Akbari M, Keijzers G, Maynard S, Scheibye-Knudsen M, Madsen CD, Hickson ID et al. Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair. DNA Repair. 2014 Apr;16:44-53. https://doi.org/10.1016/j.dnarep.2014.01.015

Author

Akbari, Mansour ; Keijzers, Guido ; Maynard, Scott ; Scheibye-Knudsen, Morten ; Madsen, Claus Desler ; Hickson, Ian D ; Bohr, Vilhelm A. / Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair. In: DNA Repair. 2014 ; Vol. 16. pp. 44-53.

Bibtex

@article{167b8dcd5cea49f8a0a34580d3f26a47,

title = "Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair",

abstract = "Base excision repair (BER) is the most prominent DNA repair pathway in human mitochondria. BER also results in a temporary generation of AP-sites, single-strand breaks and nucleotide gaps. Thus, incomplete BER can result in the generation of DNA repair intermediates that can disrupt mitochondrial DNA replication and transcription and generate mutations. We carried out BER analysis in highly purified mitochondrial extracts from human cell lines U2OS and HeLa, and mouse brain using a circular DNA substrate containing a lesion at a specific position. We found that DNA ligation is significantly slower than the preceding mitochondrial BER steps. Overexpression of DNA ligase III in mitochondria improved the rate of overall BER, increased cell survival after menadione induced oxidative stress and reduced autophagy following the inhibition of the mitochondrial electron transport chain complex I by rotenone. Our results suggest that the amount of DNA ligase III in mitochondria may be critical for cell survival following prolonged oxidative stress, and demonstrate a functional link between mitochondrial DNA damage and repair, cell survival upon oxidative stress, and removal of dysfunctional mitochondria by autophagy.",

author = "Mansour Akbari and Guido Keijzers and Scott Maynard and Morten Scheibye-Knudsen and Madsen, {Claus Desler} and Hickson, {Ian D} and Bohr, {Vilhelm A}",

note = "Copyright {\textcopyright} 2014. Published by Elsevier B.V.",

year = "2014",

month = apr,

doi = "10.1016/j.dnarep.2014.01.015",

language = "English",

volume = "16",

pages = "44--53",

journal = "DNA Repair",

issn = "1568-7864",

publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair

AU - Akbari, Mansour

AU - Keijzers, Guido

AU - Maynard, Scott

AU - Scheibye-Knudsen, Morten

AU - Madsen, Claus Desler

AU - Hickson, Ian D

AU - Bohr, Vilhelm A

PY - 2014/4

Y1 - 2014/4

N2 - Base excision repair (BER) is the most prominent DNA repair pathway in human mitochondria. BER also results in a temporary generation of AP-sites, single-strand breaks and nucleotide gaps. Thus, incomplete BER can result in the generation of DNA repair intermediates that can disrupt mitochondrial DNA replication and transcription and generate mutations. We carried out BER analysis in highly purified mitochondrial extracts from human cell lines U2OS and HeLa, and mouse brain using a circular DNA substrate containing a lesion at a specific position. We found that DNA ligation is significantly slower than the preceding mitochondrial BER steps. Overexpression of DNA ligase III in mitochondria improved the rate of overall BER, increased cell survival after menadione induced oxidative stress and reduced autophagy following the inhibition of the mitochondrial electron transport chain complex I by rotenone. Our results suggest that the amount of DNA ligase III in mitochondria may be critical for cell survival following prolonged oxidative stress, and demonstrate a functional link between mitochondrial DNA damage and repair, cell survival upon oxidative stress, and removal of dysfunctional mitochondria by autophagy.

AB - Base excision repair (BER) is the most prominent DNA repair pathway in human mitochondria. BER also results in a temporary generation of AP-sites, single-strand breaks and nucleotide gaps. Thus, incomplete BER can result in the generation of DNA repair intermediates that can disrupt mitochondrial DNA replication and transcription and generate mutations. We carried out BER analysis in highly purified mitochondrial extracts from human cell lines U2OS and HeLa, and mouse brain using a circular DNA substrate containing a lesion at a specific position. We found that DNA ligation is significantly slower than the preceding mitochondrial BER steps. Overexpression of DNA ligase III in mitochondria improved the rate of overall BER, increased cell survival after menadione induced oxidative stress and reduced autophagy following the inhibition of the mitochondrial electron transport chain complex I by rotenone. Our results suggest that the amount of DNA ligase III in mitochondria may be critical for cell survival following prolonged oxidative stress, and demonstrate a functional link between mitochondrial DNA damage and repair, cell survival upon oxidative stress, and removal of dysfunctional mitochondria by autophagy.

U2 - 10.1016/j.dnarep.2014.01.015

DO - 10.1016/j.dnarep.2014.01.015

M3 - Journal article

C2 - 24674627

VL - 16

SP - 44

EP - 53

JO - DNA Repair

JF - DNA Repair

SN - 1568-7864

ER -

ID: 108770818