**1. Introduction**

Conservation of DNA integrity is important during replication to ensure that daughter cells have accurately replicated DNA to promote genetic continuity. The accumulation of aberrations within the DNA sequence, if left unrepaired, can lead to genetic drift and subsequent detrimental effects following subsequent rounds of replication. Given that the rate of DNA replication occurs at a frequency of 500 nucleotides/minute/replication fork, only a small number of errors (~1 nucleotide per 1 × 109 nucleotides) arise during the replication process [1]. Evolution has enabled the cell to develop proof-reading mechanisms that minimise the potential disruption and preservation of its genetic code [2, 3]; however, errors remain and with time contribute to increased genomic instability and an altered metabolic landscape as required for a sufficient supply of macromolecules, including nucleotides, to drive proliferation [4–6].

Uracil is one of the most frequently occurring error bases in DNA, occurring through mutagen hydrolytic deamination of cytosine to uracil or through substantial uracil DNA misincorporation, and the cell has, therefore, evolved different strategies to target and repair this type of DNA damage. In the absence of uracil-DNA repair, relatively fast cytosine deamination and the toxicity of the resulting uracil will result in a gene drift which is likely not tolerated by an organism.
