ArticlePloS one2013
Unligated Okazaki Fragments Induce PCNA Ubiquitination and a Requirement for Rad59-Dependent Replication Fork Progression.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- The ubiquitin protease Ubp10 suppresses the formation of translocations at interstitial telomere-like sites.Nucleic acids research · 2025Article
- Functional asymmetry in processivity clamp proteins.Biophysical journal · 2025Review
- DNA lesions can frequently precede DNA:RNA hybrid accumulation.Nature communications · 2025Article
- Elevated MSH2 MSH3 expression interferes with DNA metabolism in vivo.Nucleic acids research · 2023Article
- Post-Translational Modifications of PCNA: Guiding for the Best DNA Damage Tolerance Choice.Journal of fungi (Basel, Switzerland) · 2022Review
- Fission yeast Rad8/HLTF facilitates Rad52-dependent chromosomal rearrangements through PCNA lysine 107 ubiquitination.PLoS genetics · 2021Article
- Ubiquitinated-PCNA protects replication forks from DNA2-mediated degradation by regulating Okazaki fragment maturation and chromatin assembly.Nature communications · 2020Article
- Review
- Ubiquitylation at the Fork: Making and Breaking Chains to Complete DNA Replication.International journal of molecular sciences · 2018Review
- Flap endonuclease overexpression drives genome instability and DNA damage hypersensitivity in a PCNA-dependent manner.Nucleic acids research · 2018Article
- Small molecule inhibitors uncover synthetic genetic interactions of human flap endonuclease 1 (FEN1) with DNA damage response genes.PloS one · 2017Article
- SUMOylation of Rad52-Rad59 synergistically change the outcome of mitotic recombination.DNA repair · 2016Article
- Genetic Interactions Implicating Postreplicative Repair in Okazaki Fragment Processing.PLoS genetics · 2015Article
- Replication-Coupled PCNA Unloading by the Elg1 Complex Occurs Genome-wide and Requires Okazaki Fragment Ligation.Cell reports · 2015Article
- Structurally distinct ubiquitin- and sumo-modified PCNA: implications for their distinct roles in the DNA damage response.Structure (London, England : 1993) · 2015Article
- Strand-specific analysis shows protein binding at replication forks and PCNA unloading from lagging strands when forks stall.Molecular cell · 2014Article
- Rad52/Rad59-dependent recombination as a means to rectify faulty Okazaki fragment processing.The Journal of biological chemistry · 2014Article
- Mcm10 deficiency causes defective-replisome-induced mutagenesis and a dependency on error-free postreplicative repair.Cell cycle (Georgetown, Tex.) · 2014Article
- Alleles of the homologous recombination gene, RAD59, identify multiple responses to disrupted DNA replication in Saccharomyces cerevisiae.BMC microbiology · 2013Article
- Ubiquitin and SUMO pathways in DNA replication and replication-coupled repair.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Deficiency in DNA ligase I, encoded by CDC9 in budding yeast, leads to the accumulation of unligated Okazaki fragments and triggers PCNA ubiquitination at a non-canonical lysine residue. This signal is crucial to activate the S phase checkpoint, which promotes cell cycle delay. We report here that a pol30-K107 mutation alleviated cell cycle delay in cdc9 mutants, consistent with the idea that the modification of PCNA at K107 affects the rate of DNA synthesis at replication forks. To determine whether PCNA ubiquitination occurred in response to nicks or was triggered by the lack of PCNA-DNA ligase interaction, we complemented cdc9 cells with either wild-type DNA ligase I or a mutant form, which fails to interact with PCNA. Both enzymes reversed PCNA ubiquitination, arguing that the modification is likely an integral part of a novel nick-sensory mechanism and not due to non-specific secondary mutations that could have occurred spontaneously in cdc9 mutants. To further understand how cells cope with the accumulation of nicks during DNA replication, we utilized cdc9-1 in a genome-wide synthetic lethality screen, which identified RAD59 as a strong negative interactor. In comparison to cdc9 single mutants, cdc9 rad59Δ double mutants did not alter PCNA ubiquitination but enhanced phosphorylation of the mediator of the replication checkpoint, Mrc1. Since Mrc1 resides at the replication fork and is phosphorylated in response to fork stalling, these results indicate that Rad59 alleviates nick-induced replication fork slowdown. Thus, we propose that Rad59 promotes fork progression when Okazaki fragment processing is compromised and counteracts PCNA-K107 mediated cell cycle arrest.
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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.