Journal
NATURE
Volume 456, Issue 7224, Pages 915-920Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature07587
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Funding
- Associazione Italiana per la Ricerca sul Cancro
- Association for International Cancer Research
- European Community GENICA
- European Community DNA Repair
- Telethon
- MIUR
- Ministry of Health
- Buzzati-Traverso foundation
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Replication by template switch is thought to mediate DNA damage- bypass and fillings of gaps. Gap- filling repair requires homologous recombination as well as Rad18- and Rad5- mediated proliferating cell nuclear antigen ( PCNA) polyubiquitylation. However, it is unclear whether these processes are coordinated, and the physical evidence for Rad18 - Rad5- dependent template switch at replication forks is still elusive. Here we show, using genetic and physical approaches, that in budding yeast ( Saccharomyces cerevisiae) Rad18 is required for the formation of X- shaped sister chromatid junctions ( SCJs) at damaged replication forks through a process involving PCNA polyubiquitylation and the ubiquitin- conjugating enzymes Mms2 and Ubc13. The Rad18 - Mms2- mediated damage- bypass through SCJs requires the small ubiquitin- like modifier ( SUMO)- conjugating enzyme Ubc9 and SUMOylated PCNA, and is coordinated with Rad51- dependent recombination events. We propose that the Rad18 - Rad5 - Mms2- dependent SCJs represent template switch events. Altogether, our results unmask a role for PCNA ubiquitylation and SUMOylation pathways in promoting transient damage- induced replication- coupled recombination events involving sister chromatids at replication forks.
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