Practice question

Translesion DNA synthesis represents damage tolerance mechanism allowing replication fork to bypass bulky adducts, pyrimidine dimers, cisplatin crosslinks, or apurinic sites that block high-fidelity replicative polymerases. Specialized Y-family polymerases Pol IV and Pol V possess capacious active sites accommodating distorted base pairs but lack 3' to 5' proofreading exonuclease and exhibit relaxed Watson-Crick selection. As result, they insert nucleotides opposite lesions with high misincorporation rates, generating targeted and untargeted mutations in SOS response. Though mutagenic, TLS prevents double-strand breaks caused by fork collapse and enhances survival under genotoxic stress.