ArticleNucleic acids research2019
Rad5 dysregulation drives hyperactive recombination at replication forks resulting in cisplatin sensitivity and genome instability.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- S-phase checkpoint protects from aberrant replication fork processing and degradation.Nucleic acids research · 2025Article
- The DNA damage tolerance factor Rad5 and telomere replication.Current genetics · 2025Review
- Repair of replication-dependent double-strand breaks differs between the leading and lagging strands.Molecular cell · 2025Article
- HLTF Promotes the Proliferation of Osteosarcoma Cells and Cisplatin Resistance.Anti-cancer agents in medicinal chemistry · 2025Article
- Aberrant DNA repair reveals a vulnerability in histone H3.3-mutant brain tumors.Nucleic acids research · 2024Article
- Mechanism for inverted-repeat recombination induced by a replication fork barrier.Nature communications · 2022Article
- Rad5 participates in lesion bypass through its Rev1-binding and ubiquitin ligase domains, but not through its helicase function.Frontiers in molecular biosciences · 2022Article
- A role for Rad5 in ribonucleoside monophosphate (rNMP) tolerance.Life science alliance · 2021Article
- Fission yeast Rad8/HLTF facilitates Rad52-dependent chromosomal rearrangements through PCNA lysine 107 ubiquitination.PLoS genetics · 2021Article
- Structural basis for the multi-activity factor Rad5 in replication stress tolerance.Nature communications · 2021Article
- Lysine acetylation regulates the activity of nuclear Pif1.The Journal of biological chemistry · 2020Article
- Time for remodeling: SNF2-family DNA translocases in replication fork metabolism and human disease.DNA repair · 2020Review
- Contractions of the C-Terminal Domain ofG3 (Bethesda, Md.) · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The postreplication repair gene, HLTF, is often amplified and overexpressed in cancer. Here we model HLTF dysregulation through the functionally conserved Saccharomyces cerevisiae ortholog, RAD5. Genetic interaction profiling and landscape enrichment analysis of RAD5 overexpression (RAD5OE) reveals requirements for genes involved in recombination, crossover resolution, and DNA replication. While RAD5OE and rad5Δ both cause cisplatin sensitivity and share many genetic interactions, RAD5OE specifically requires crossover resolving genes and drives recombination in a region of repetitive DNA. Remarkably, RAD5OE induced recombination does not require other post-replication repair pathway members, or the PCNA modification sites involved in regulation of this pathway. Instead, the RAD5OE phenotype depends on a conserved domain necessary for binding 3' DNA ends. Analysis of DNA replication intermediates supports a model in which dysregulated Rad5 causes aberrant template switching at replication forks. The direct effect of Rad5 on replication forks in vivo, increased recombination, and cisplatin sensitivity predicts similar consequences for dysregulated HLTF in cancer.
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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.