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  Absence of mitochondrial SLC25A51 enhances PARP1-dependent DNA repair by increasing nuclear NAD+ levels

Güldenpfennig, A., Hopp, A.-K., Muskalla, L., Manetsch, P., Raith, F., Hellweg, L., et al. (2023). Absence of mitochondrial SLC25A51 enhances PARP1-dependent DNA repair by increasing nuclear NAD+ levels. Nucleic Acids Research, 51(17), 9248-9265. doi:10.1093/nar/gkad659.

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Item Permalink: https://hdl.handle.net/21.11116/0000-000D-DD8F-A Version Permalink: https://hdl.handle.net/21.11116/0000-000D-DD90-7
Genre: Journal Article

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 Creators:
Güldenpfennig, Anka, Author
Hopp, Ann-Katrin, Author
Muskalla, Lukas, Author
Manetsch, Patrick, Author
Raith, Fabio1, Author           
Hellweg, Lars, Author
Dördelmann, Cyril, Author
Pedrioli, Deena M Leslie, Author
Johnsson, Kai2, Author           
Superti-Furga, Giulio, Author
Hottiger, Michael O, Author
Affiliations:
1Cellular Biophysics, Max Planck Institute for Medical Research, Max Planck Society, ou_2364731              
2Chemical Biology, Max Planck Institute for Medical Research, Max Planck Society, ou_2364732              

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 Abstract: Though the effect of the recently identified mitochondrial NAD+ transporter SLC25A51 on glucose metabolism has been described, its contribution to other NAD+-dependent processes throughout the cell such as ADP-ribosylation remains elusive. Here, we report that absence of SLC25A51 leads to increased NAD+ concentration not only in the cytoplasm and but also in the nucleus. The increase is not associated with upregulation of the salvage pathway, implying an accumulation of constitutively synthesized NAD+ in the cytoplasm and nucleus. This results in an increase of PARP1-mediated nuclear ADP-ribosylation, as well as faster repair of DNA lesions induced by different single-strand DNA damaging agents. Lastly, absence of SLC25A51 reduces both MMS/Olaparib induced PARP1 chromatin retention and the sensitivity of different breast cancer cells to PARP1 inhibition. Together these results provide evidence that SLC25A51 might be a novel target to improve PARP1 inhibitor based therapies by changing subcellular NAD+ redistribution.

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Language(s): eng - English
 Dates: 2023-07-162023-01-132023-07-312023-08-172023-09-22
 Publication Status: Issued
 Pages: 18
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1093/nar/gkad659
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Title: Nucleic Acids Research
  Other : Nucleic Acids Res
Source Genre: Journal
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Publ. Info: Oxford : Oxford University Press
Pages: - Volume / Issue: 51 (17) Sequence Number: - Start / End Page: 9248 - 9265 Identifier: ISSN: 0305-1048
CoNE: https://pure.mpg.de/cone/journals/resource/110992357379342