Evolutionary origins of dna repair pathways: Role of oxygen catastrophe in the emergence of dna glycosylases


Prorok P. Grin I.R. Matkarimov B.T. Ishchenko A.A. Laval J. Zharkov D.O. Saparbaev M.
July 2021MDPI

Cells
2021#10Issue 7

It was proposed that the last universal common ancestor (LUCA) evolved under high temperatures in an oxygen-free environment, similar to those found in deep-sea vents and on volcanic slopes. Therefore, spontaneous DNA decay, such as base loss and cytosine deamination, was the major factor affecting LUCA’s genome integrity. Cosmic radiation due to Earth’s weak magnetic field and alkylating metabolic radicals added to these threats. Here, we propose that ancient forms of life had only two distinct repair mechanisms: versatile apurinic/apyrimidinic (AP) endonucleases to cope with both AP sites and deaminated residues, and enzymes catalyzing the direct reversal of UV and alkylation damage. The absence of uracil–DNA N-glycosylases in some Archaea, together with the presence of an AP endonuclease, which can cleave uracil-containing DNA, suggests that the AP endonuclease-initiated nucleotide incision repair (NIR) pathway evolved independently from DNA glycosylase-mediated base excision repair. NIR may be a relic that appeared in an early thermophilic ancestor to counteract spontaneous DNA damage. We hypothesize that a rise in the oxygen level in the Earth’s atmosphere ~2 Ga triggered the narrow specialization of AP endonucleases and DNA glycosylases to cope efficiently with a widened array of oxidative base damage and complex DNA lesions.

AP endonucleases , DNA glycosylases , DNA repair , Protein folds , Structural homology

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Department of Biology, Technical University of Darmstadt, Darmstadt, 64287, Germany
SB RAS Institute of Chemical Biology and Fundamental Medicine, 8 Lavrentieva Ave., Novosibirsk, 630090, Russian Federation
Center for Advanced Biomedical Research, Department of Natural Sciences, Novosibirsk State University, 2 Pirogova St., Novosibirsk, 630090, Russian Federation
National Laboratory Astana, Nazarbayev University, Nur-Sultan, 010000, Kazakhstan
Groupe «Mechanisms of DNA Repair and Carcinogenesis», Equipe Labellisée LIGUE 2016, CNRS UMR9019, Université Paris-Saclay, Gustave Roussy Cancer Campus, Villejuif, F-94805, France

Department of Biology
SB RAS Institute of Chemical Biology and Fundamental Medicine
Center for Advanced Biomedical Research
National Laboratory Astana
Groupe «Mechanisms of DNA Repair and Carcinogenesis»

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