Hat both the mutant and wild-type Pol bound to monoubiquitinated PCNA in BPDE-treated cells, indicating that at least one of the two ubiquitin-binding domains (designated UBZs) was involved in the binding. This result eliminates a trivial explanation that the reduced REV1-binding activity of the Pol mutant protein is due to failure in protein folding. Thus, we conclude that the interaction with RE