<p>DNA damage stalls the replication complex and triggers the ubiquitylation of PCNA by Rad6–Rad18 at the stalled fork. Monoubiquitylated PCNA promotes TLS, for which to occur first Pol3 is removed from the stalled complex through ubiquitylation-mediated proteasomal degradation, assisted by Def1. A TLS polymerase takes over the place of Pol3, and together with Pol31 and Pol32 carries out lesion bypass. After the deubiquitylation of PCNA, Pol3 regains its place at the replication complex, and normal replication resumes. For simplicity, only half of the replication fork is shown. The DNA damage site on the template strand is marked by a black diamond symbol.</p
