Journal
EMBO JOURNAL
Volume 29, Issue 12, Pages 2048-2058Publisher
WILEY
DOI: 10.1038/emboj.2010.87
Keywords
post-replicative repair; translesion synthesis; ubiquitin ligase Rad6-Rad18; ubiquitin ligase Rad8(Rad5)/Ubc13-Mms2; UV photoproducts
Categories
Funding
- Agence Nationale de la Recherche [ANR-06-BLAN-0258]
- MRC
- EC RTN
- 'Association pour la Recherche sur le Cancer' (ARC)
- MRC [G0501450] Funding Source: UKRI
- Medical Research Council [G0801130B, G0501450] Funding Source: researchfish
- Agence Nationale de la Recherche (ANR) [ANR-06-BLAN-0258] Funding Source: Agence Nationale de la Recherche (ANR)
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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 Pol eta or Pol zeta, 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. The EMBO Journal (2010) 29, 2048-2058. doi: 10.1038/emboj.2010.87; Published online 7 May 2010
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