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Rad8 Rad5 /Mms2–Ubc13 ubiquitin ligase complex controls translesion synthesis in fission yeast
Author(s) -
Coulon Stéphane,
Ramasubramanyan Sharada,
Alies Carole,
Philippin Gaëlle,
Lehmann Alan,
Fuchs Robert P
Publication year - 2010
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2010.87
Subject(s) - proliferating cell nuclear antigen , schizosaccharomyces pombe , ubiquitin , biology , ubiquitin ligase , microbiology and biotechnology , postreplication repair , dna ligase , dna damage , saccharomyces cerevisiae , schizosaccharomyces , dna repair , dna replication , biochemistry , ubiquitin conjugating enzyme , dna , yeast , nucleotide excision repair , gene
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 Polη or Polζ, 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.