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Abstract

DNA lesions can be eliminated from metazoan organisms by DNA repair processes or by cell death. If DNA damage remains unrepaired and cells survive, the efficiency and fidelity of essential nuclear functions is seriously threatened. In particular, replication of damaged DNA represents a major mechanism of genetic instability.1,2 Covalent modification of DNA bases may disrupt the hydrogen bonding information and generate noninstructional sites. During subsequent DNA replication, damaged templates are unable to mediate the recruitment of complementary deoxyribonucleotides using their hydrogen-bonding pattern and, in many cases, DNA polymerases have only a 25% probability of adding the correct base. As a general rule, DNA polymerases tend to select purines, preferentially adenine residues, across such noninstructional sites.3

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Naegeli, H. (1997). Recognition of DNA Damage During Replication. In: Mechanisms of DNA Damage Recognition in Mammalian Cells. Molecular Biology Intelligence Unit. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-6468-9_10

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