ArticleThe EMBO journal2014
DNA bending facilitates the error-free DNA damage tolerance pathway and upholds genome integrity.
Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed.
- Exploiting DNA damage tolerance for precision oncology.Trends in cancer · 2026Review
- The Yeast HMGB Protein Hmo1 Is a Multifaceted Regulator of DNA Damage Tolerance.International journal of molecular sciences · 2025Article
- Hmo1: A versatile member of the high mobility group box family of chromosomal architecture proteins.World journal of biological chemistry · 2024Review
- Implications of ubiquitination and the maintenance of replication fork stability in cancer therapy.Bioscience reports · 2023Review
- Targeting of Hmo1 to subcompartments of the budding yeast nucleolus.Molecular biology of the cell · 2023Article
- Implications of Translesion DNA Synthesis Polymerases on Genomic Stability and Human Health.Molecular and cellular biology · 2023Article
- DNA Holliday Junction: History, Regulation and Bioactivity.International journal of molecular sciences · 2022Review
- Post-Translational Modifications of PCNA: Guiding for the Best DNA Damage Tolerance Choice.Journal of fungi (Basel, Switzerland) · 2022Review
- Rad51-mediated replication of damaged templates relies on monoSUMOylated DDK kinase.Nature communications · 2022Article
- Temporally distinct post-replicative repair mechanisms fill PRIMPOL-dependent ssDNA gaps in human cells.Molecular cell · 2021Article
- Smc5/6 functions with Sgs1-Top3-Rmi1 to complete chromosome replication at natural pause sites.Nature communications · 2021Article
- Short-range template switching in great ape genomes explored using pair hidden Markov models.PLoS genetics · 2021Article
- To skip or not to skip: choosing repriming to tolerate DNA damage.Molecular cell · 2021Review
- Participation of the HIM1 gene of yeast Saccharomyces cerevisiae in the error-free branch of post-replicative repair and role Polη in him1-dependent mutagenesis.Current genetics · 2021Article
- DNA Damage Tolerance Pathways in Human Cells: A Potential Therapeutic Target.Frontiers in oncology · 2021Review
- Prevention of unwanted recombination at damaged replication forks.Current genetics · 2020Review
- Mus81-Mms4 endonuclease is an Esc2-STUbL-Cullin8 mitotic substrate impacting on genome integrity.Nature communications · 2020Article
- Article
- Effects of chain length and geometry on the activation of DNA damage bypass by polyubiquitylated PCNA.Nucleic acids research · 2020Article
- Replication Fork Remodeling and Therapy Escape in DNA Damage Response-Deficient Cancers.Frontiers in oncology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
DNA replication is sensitive to damage in the template. To bypass lesions and complete replication, cells activate recombination-mediated (error-free) and translesion synthesis-mediated (error-prone) DNA damage tolerance pathways. Crucial for error-free DNA damage tolerance is template switching, which depends on the formation and resolution of damage-bypass intermediates consisting of sister chromatid junctions. Here we show that a chromatin architectural pathway involving the high mobility group box protein Hmo1 channels replication-associated lesions into the error-free DNA damage tolerance pathway mediated by Rad5 and PCNA polyubiquitylation, while preventing mutagenic bypass and toxic recombination. In the process of template switching, Hmo1 also promotes sister chromatid junction formation predominantly during replication. Its C-terminal tail, implicated in chromatin bending, facilitates the formation of catenations/hemicatenations and mediates the roles of Hmo1 in DNA damage tolerance pathway choice and sister chromatid junction formation. Together, the results suggest that replication-associated topological changes involving the molecular DNA bender, Hmo1, set the stage for dedicated repair reactions that limit errors during replication and impact on genome stability.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.