(E) Model for Rad52-mediated tolerance during DDT. The recombination factors Rad52, Rad51 and Rad57 promote efficient Rad6/Rad18 binding to chromatin under unperturbed conditions. In response to blocking lesions that impair replication fork advance the Rad6/Rad18 complex is mobilized to ssDNA lesions where, together with Mms2/Ubc13/Rad5, ubiquitylates PCNA and promotes TS. The ssDNA lesions that escape from this error-free pathway during S phase accumulate in G2/M, where they are filled in by two additional, less accurate mechanisms regulated by Rad52: UbPCNA-independent HR (recombinogenic) and TLS (mutagenic). Apart from facilitating Rad6/Rad18 chromatin recruitment, Rad52 plays an additional uncharacterized Rad51/Rad57-independent role in TLS. 