Abstract：
:In addition to its role as an electron transporter, mitochondrial nicotinamide adenine dinucleotide (NAD+) is an important co-factor for enzymatic reactions, including ADP-ribosylation. Although mitochondria harbor the most intra-cellular NAD+, mitochondrial ADP-ribosylation remains poorly understood. Here we provide evidence for mitochondrial ADP-ribosylation, which was identified using various methodologies including immunofluorescence, western blot, and mass spectrometry. We show that mitochondrial ADP-ribosylation reversibly increases in response to respiratory chain inhibition. Conversely, H2O2-induced oxidative stress reciprocally induces nuclear and reduces mitochondrial ADP-ribosylation. Elevated mitochondrial ADP-ribosylation, in turn, dampens H2O2-triggered nuclear ADP-ribosylation and increases MMS-induced ARTD1 chromatin retention. Interestingly, co-treatment of cells with the mitochondrial uncoupler FCCP decreases PARP inhibitor efficacy. Together, our results suggest that mitochondrial ADP-ribosylation is a dynamic cellular process that impacts nuclear ADP-ribosylation and provide evidence for a NAD+-mediated mitochondrial-nuclear crosstalk.
journal_name
Mol Celljournal_title
Molecular cellauthors
Hopp AK,Teloni F,Bisceglie L,Gondrand C,Raith F,Nowak K,Muskalla L,Howald A,Pedrioli PGA,Johnsson K,Altmeyer M,Pedrioli DML,Hottiger MOdoi
10.1016/j.molcel.2020.12.034subject
Has Abstractpub_date
2021-01-21 00:00:00pages
340-354.e5issue
2eissn
1097-2765issn
1097-4164pii
S1097-2765(20)30955-2journal_volume
81pub_type
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