ArticleCell cycle (Georgetown, Tex.)2016
Coordination of DNA damage tolerance mechanisms with cell cycle progression in fission yeast.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- The relationship between DNA damage and repair and the occurrence and development of disease.Frontiers in genetics · 2026Review
- Translesion synthesis polymerases contribute to meiotic chromosome segregation and cohesin dynamics inJournal of cell science · 2020Article
- Dynamics of DNA replication in a eukaryotic cell.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Mathematical description of eukaryotic chromosome replication.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Solution NMR structure of the HLTF HIRAN domain: a conserved module in SWI2/SNF2 DNA damage tolerance proteins.Journal of biomolecular NMR · 2016Article
- Non mutagenic and mutagenic DNA damage tolerance.Cell cycle (Georgetown, Tex.) · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA damage tolerance (DDT) mechanisms allow cells to synthesize a new DNA strand when the template is damaged. Many mutations resulting from DNA damage in eukaryotes are generated during DDT when cells use the mutagenic translesion polymerases, Rev1 and Polζ, rather than mechanisms with higher fidelity. The coordination among DDT mechanisms is not well understood. We used live-cell imaging to study the function of DDT mechanisms throughout the cell cycle of the fission yeast Schizosaccharomyces pombe. We report that checkpoint-dependent mitotic delay provides a cellular mechanism to ensure the completion of high fidelity DDT, largely by homology-directed repair (HDR). DDT by mutagenic polymerases is suppressed during the checkpoint delay by a mechanism dependent on Rad51 recombinase. When cells pass the G2/M checkpoint and can no longer delay mitosis, they completely lose the capacity for HDR and simultaneously exhibit a requirement for Rev1 and Polζ. Thus, DDT is coordinated with the checkpoint response so that the activity of mutagenic polymerases is confined to a vulnerable period of the cell cycle when checkpoint delay and HDR are not possible.
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Registered trials
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