Many DNA lesions cause pausing of replication forks at lesion sites; thus, 
generating gaps in the daughter strands that are filled-in by post-replication 
repair (PRR) pathways. In Saccharomyces cerevisiae, PRR involves translesion 
synthesis (TLS) mediated by Poleta or Polzeta, or Rad5-dependent gap filling 
through a poorly characterized error-free mechanism. We have developed an assay 
to monitor error-free and mutagenic TLS across single DNA lesions in 
Schizosaccharomyces pombe. For both main UV photolesions, we have delineated a 
major error-free pathway mediated by a distinct combination of TLS polymerases. 
Surprisingly, these TLS pathways require enzymes needed for poly-ubiquitination 
of proliferating cell nuclear antigen (PCNA) as well as those required for 
mono-ubiquitination. For pathways that require several TLS polymerases the 
poly-ubiquitin chains of PCNA may facilitate their recruitment through specific 
interactions with their multiple ubiquitin-binding motifs. These error-free TLS 
pathways may at least partially account for the previously described 
poly-ubiquitination-dependent error-free branch of PRR. This work highlights 
major differences in the control of lesion tolerance pathways between S. pombe 
and S. cerevisiae despite the homologous sets of PRR genes these organisms 
share.