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Genomic DNA is susceptible to a variety of mutagenic processes. The maintenance of the stability of genetic material, which is an important and essential feature of every living or‐ ganism, depends on an accurate DNA replication [1]. Organisms across all kingdoms have developed diverse and highly efficient repair mechanisms to safeguard the genome from deleterious consequences of various kinds of stresses that might tend to destabilize the in‐ tegrity of the genome. DNA is constantly being damaged. A low fidelity of DNA synthesis in various compartments of the cells by main replicative DNA polymerases leads to genom‐ ic instability (mutator phenotype) [2]. The errors produced during DNA synthesis could re‐ sult from three fidelity determining processes: a)nucleotide misinsertion into the nascent DNA, b)lack of exonucleolytic proofreading activity, i.e the mechanism to identify and ex‐ cise incorrect nucleotide incorporated during DNA synthesis, and c)extension of mismatch‐ ed 3’-termini of DNA [3]. Failure to repair DNA can lead to mutations, genomic instability, chromosomal abnormalities, progression of cancer and premature aging.

The Role of P53 Exonuclease in Accuracy of DNA Synthesis and Sensitivity to Nucleoside Analogs in Various Compartments of Cells