Rev1 Background Information Cells subjected to irradiation with ultraviolet light (UV) suffer DNA damage in the form of covalent linkage between adjacent pyrimidines (1). DNA repair can occur in either an error-free mechanism, which has the ability to correctly replicate past the lesion, or via an error-prone mechanism, which replicates DNA despite an unrepaired lesion (1,2). The error-prone mechanism is referred to as translesion synthesis (TLS) and it has the ability to incorporate new mutations into the genome, which is a potential origin of cancer (1,2). Rad30 (also designated DNA polymerase h (Pol h) or xeroderma pigmentosum variant (XPV)) is able to replicate in an error-free manner past a cis-syn-thymine-thymine dimer in S. cerevisiae (3). The Rev1, Rev3, and Rev 7 proteins are the subunits of DNA polymerase z (Pol-z), which is involved in translesion synthesis (4). In S. cerevisiae, Rnr1 is a ribonucleotide reductase that catalyzes the rate-limiting step in the production of deoxyribonucleotides essential for DNA synthesis and repair (5).
