PCNA ubiquitination and REV1 define temporally distinct mechanisms for controlling translesion synthesis in the avian cell line DT40.

摘要: Translesion synthesis (TLS) is a potentially mutagenic method of bypassing DNA damage encountered during replication that requires the recruitment specialized polymerases to stalled forks or postreplicative gaps. Current models suggest TLS activated by monoubiquitination sliding clamp PCNA. However, in higher organisms, fully effective also noncatalytic function Y family polymerase REV1. Using genetically tractable chicken cell line DT40, we show at both translesion polymerase-interaction domain and ubiquitin-binding C terminus REV1 are intact. Surprisingly, however, PCNA ubiquitination not required maintain normal fork progression on damaged DNA. Conversely, essential for filling Thus, play distinct roles coordination bypass temporally separated relative arrest.