ArticleMitochondrial DNA. Part A, DNA mapping, sequencing, and analysis2016
The efficiency of the translesion synthesis across abasic sites by mitochondrial DNA polymerase is low in mitochondria of 3T3 cells.
Article in Mitochondrial DNA. Part A, DNA mapping, sequencing, and analysis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- DNA repair pathways in the mitochondria.DNA repair · 2025Review
- Dual chemical labeling enables nucleotide-resolution mapping of DNA abasic sites and common alkylation damage in human mitochondrial DNA.Nucleic acids research · 2023Article
- Key Amino Acid Residues of Mitochondrial Transcription Factor A Synergize with Abasic (AP) Site Dynamics To Facilitate AP-Lyase Reactions.ACS chemical biology · 2023Article
- DNA-protein cross-links between abasic DNA damage and mitochondrial transcription factor A (TFAM).Nucleic acids research · 2023Article
- Transient State Kinetics ofBiochemistry · 2022Article
- Beyond base excision repair: an evolving picture of mitochondrial DNA repair.Bioscience reports · 2021Review
- Mitochondrial transcription factor A promotes DNA strand cleavage at abasic sites.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Mitochondrial DNA degradation: A quality control measure for mitochondrial genome maintenance and stress response.The Enzymes · 2019Review
- Increased TFAM binding to mtDNA damage hot spots is associated with mtDNA loss in aged rat heart.Free radical biology & medicine · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Translesion synthesis by specialized DNA polymerases is an important strategy for mitigating DNA damage that cannot be otherwise repaired either due to the chemical nature of the lesion. Apurinic/Apyrimidinic (abasic, AP) sites represent a block to both transcription and replication, and are normally repaired by the base excision repair (BER) pathway. However, when the number of abasic sites exceeds BER capacity, mitochondrial DNA is targeted for degradation. Here, we used two uracil-N-glycosylase (UNG1) mutants, Y147A or N204D, to generate AP sites directly in the mtDNA of NIH3T3 cells in vivo at sites normally occupied by T or C residues, respectively, and to study repair of these lesions in their native context. We conclude that mitochondrial DNA polymerase γ (Pol γ) is capable of translesion synthesis across AP sites in mitochondria of the NIH3T3 cells, and obeys the A-rule. However, in our system, base excision repair (BER) and mtDNA degradation occur more frequently than translesion bypass of AP sites.
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Registered trials
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