Abstract
The presence of DNA damage can increase the likelihood of DNA replication errors and promote mutations. In particular, pauses of DNA polymerase at the site of damage can lead to polymerase slippage and the formation of 1–2-nucleotide bulges. Repair of such structures using an undamaged DNA template leads to small deletions. One of the most abundant oxidative DNA lesions, 8-oxoguanine (oxoG), was shown to induce small deletions, but the mechanism of this phenomenon is currently unknown. We studied the aberrant repair of oxoG located in one- and two-nucleotide bulges by the Escherichia coli and human base excision repair systems. Our results indicate that the repair in such substrates can serve as a mechanism for fixing small deletions in bacteria but not in humans.
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ACKNOWLEDGMENTS
DNA sequencing was performed by employees of the Genomics Core Facility (Siberian Branch, Russian Academy of Sciences). Nfo protein was kindly provided by A.A. Ishchenko (Paris-Saclay University , France).
Funding
The work was supported by the Russian Foundation for Basic Research (project no. 21-54-12025 NNIO_a).
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Translated by M. Batrukova
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Eroshenko, D.A., Diatlova, E.A., Golyshev, V.M. et al. Aberrant Repair of 8-Oxoguanine in Short DNA Bulges. Dokl Biochem Biophys 513 (Suppl 1), S82–S86 (2023). https://doi.org/10.1134/S1607672923600355
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DOI: https://doi.org/10.1134/S1607672923600355