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Abasic Site Repair in Higher Eukaryotes

  • Chapter
DNA Damage and Repair

Part of the book series: Contemporary Cancer Research ((CCR))

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Abstract

Base-excision repair (BER) refers to a repair pathway that generates and repairs abasic sites in double-stranded (ds) DNA (Fig. 1) (101,134,222,264). BER is important not only in maintaining the integrity of nuclear DNA but also in protecting mitochondrial DNA against oxidative onslaught from FADH2 and NADH and the reactive oxygen species generated during O2 reduction (42). Estimates of the number of abasic sites generated per mammalian cell per day run as high as 106/cell/d (88). Abasic sites are unstable, degrading spontaneously into DNA strand-breaks by β-elimination (132) that retard DNA polymerases (43,44,50,66,91,237). They are highly mutagenic because of nontemplated DNA (59,108,273) and RNA (66,216,217,283) synthesis. Moreover, abasic sites engage in suicide reactions with topoisomerase I, leading to permanent DNA damage and premature cell death (196) and can form covalent complexes with topoisomerase II that cause DNA double-strand breaks (107), which can bind poly (ADP-ribose) polymerase (2,152,153). Despite the large number of abasic sites generated per cell per day, the number of resulting mutations is extremely low. The difference reflects the elaborate mechanisms that the cell has devised to repair abasic sites (134).

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  1. Phyllis R. Strauss
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  1. Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Albuquerque, NM, USA

    Jac A. Nickoloff

  2. Qbiogene, Carlsbad, CA, USA

    Merl F. Hoekstra

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Strauss, P.R., O’Regan, N.E. (2001). Abasic Site Repair in Higher Eukaryotes. In: Nickoloff, J.A., Hoekstra, M.F. (eds) DNA Damage and Repair. Contemporary Cancer Research. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-095-7_3

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