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¹ Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980–8578, Japan
² Genetic Dynamics Research Unit Laboratory, RIKEN Research Institute, Wako, Saitama, 351–0198, Japan

Ubiquitination of proteins was previously shown to modulate various processes of DNA metabolism. PCNA, a processivity factor with essential functions in replication and repair, is modified with ubiquitin at K164. In addition, PCNA is sumoylated at K127 and K164. We found that the rad18 mutation suppresses the temperature sensitivity of the polymerase  mutants hys2-1 and cdc2-1 as well as the synthetic lethality of cdc2-1 pol32 mutants, suggesting a role for Rad18 in modulating DNA replication. As Rad18 mediates ubiquitination of PCNA, we examined whether PCNA modifications affected its function in replication. Multicopy PCNA alleviated the replication defects of rfc5-1 strains, but not those of pol mutants. In contrast, multicopy PCNA-K164R had reduced ability to suppress the replication defects of rfc5-1, but alleviated those of pol mutants. The roles of sumoylated and ubiquitinated PCNA in rfc5-1 and hys2-1 mutants were addressed by using mutant backgrounds that selectively affected sumoylation (siz1), ubiquitination (rad18), polyubiquitination (rad5, mms2), or the ability of cells to perform translesion synthesis (pol, pol). Our results are consistent with the idea that the Rad18/Rad5/Mms2 polyubiquitination pathway is important for replication completion, perhaps by promoting a template switch type of DNA synthesis.

^* Correspondence: Email: branzei{at}postman.riken.go.jp

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