The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Ubiquitin-dependent DNA damage bypass is separable from genome replication
Open accessAbstract
Post-replication repair (PRR) is a pathway that allows cells to bypass or overcome lesions during DNA replication. In eukaryotes, damage bypass is activated by ubiquitylation of the replication clamp PCNA through components of the RAD6 pathway. Whereas monoubiquitylation of PCNA allows mutagenic translesion synthesis by damage-tolerant DNA polymerases, polyubiquitylation is required for an error-free pathway that probably involves a template switch to the undamaged sister chromatid. Both the timing of PRR events during the cell cycle and their location relative to replication forks, as well as the factors required downstream of PCNA ubiquitylation, have remained poorly characterized. Here we demonstrate that the RAD6 pathway normally operates during S phase. However, using an inducible system of DNA damage bypass in budding yeast (Saccharomyces cerevisiae), we show that the process is separable in time and space from genome replication, thus allowing direct visualization and quantification of productive PRR tracts. We found that both during and after S phase ultraviolet-radiation-induced lesions are bypassed predominantly via translesion synthesis, whereas the error-free pathway functions as a backup system. Our approach has revealed the distribution of PRR tracts in a synchronized cell population. It will allow an in-depth mechanistic analysis of how cells manage the processing of lesions to their genomes during and after replication.
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“In these conditions, repair may not be completed and the extension of the ssDNA region may meet two purposes: activating the checkpoint response and channeling the problematic lesion to a different repair pathway (e.g., recombination) [66–68].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [67]
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“In fact, S phase can be completed in the absence of PRR, but the gapped replicated DNA needs to be refilled by PRR in G2 in order to warrant cell survival [66,67].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [67]
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Metadata
- Authors
- Daigaku, Y., Davies, A. A., & Ulrich, H. D.
- Affiliations
- Cancer Research UK (GB)
- Corresponding author
- Ulrich, Helle D.
- Venue
- Nature
- Published
- 2010-05-09
- Volume
- 465
- Issue
- 7300
- Pages
- 951-955
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC2888004
- OpenAlex
- W2080574942
- Cited by
- 259
- References
- 30
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 9 · 2023: 4 · 2022: 6 · 2021: 15 · 2020: 15 · 2019: 13 · 2018: 21 · 2017: 16 · 2016: 26 · 2015: 15 · 2014: 18 · 2013: 22 · 2012: 27
- FWCI
- 11.08
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Cancer Research UK (A7123, A10152)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- DNA damage bypass, translesion synthesis, error-free bypass, genome replication, S phase, Saccharomyces cerevisiae, replication fork, DNA polymerase, monoubiquitylation, polyubiquitination, template switching, sister chromatids, cell cycle synchronization
- MeSH terms
- Cell Cycle, Chromatin, DNA Damage, DNA Replication, Saccharomyces cerevisiae, Time Factors, Ultraviolet Rays, Genome, Proliferating Cell Nuclear Antigen, Ubiquitin, Saccharomyces cerevisiae Proteins, Ubiquitin-Conjugating Enzymes
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