Post-replication repair (PRR) mechanisms operate to either excise or bypass lesions in the DNA that can stall progression of the replication fork. An important step in PRR is the ubiquifmation of proliferating cell nuclear antigen (PCNA) that serves as the sliding clamp/processivity factor for the replicative polymerases during DNA replication. It has been previously reported that monoubiquitinated PCNA has increased affinity for the TLS polymerases and hence, can stimulate the activity of the polymerases to by-pass replication stalling lesions (translesion synthesis) in the DNA.