ArticlePLoS genetics2021
Limiting DNA polymerase delta alters replication dynamics and leads to a dependence on checkpoint activation and recombination-mediated DNA repair.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- RECQ4 arginine methylation suppresses single-stranded DNA gap accumulation at replication forks.Nucleic acids research · 2026Article
- Eukaryotic Lagging Strand Synthesis is Distributive.bioRxiv : the preprint server for biology · 2025Article
- Recombination-coupled DNA synthesis facilitates post-invasion steps in meiotic crossover and noncrossover formations.Nucleic acids research · 2025Article
- The DNA replication checkpoint limits Okazaki fragment accumulation to protect and restart stalled forks.Molecular cell · 2025Article
- Equivocating and Deliberating on the Probability of COVID-19 Infection Serving as a Risk Factor for Lung Cancer and Common Molecular Pathways Serving as a Link.Pathogens (Basel, Switzerland) · 2024Review
- Dominant and genome-wide formation of DNA:RNA hybrid G-quadruplexes in living yeast cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- COVID-19: An overview on possible transmission ways, sampling matrices and diagnosis.BioImpacts : BI · 2024Review
- Cellular state landscape and herpes simplex virus type 1 infection progression are connected.Nature communications · 2023Article
- Post-replicative nick translation occurs on the lagging strand during prolonged depletion of DNA ligase I in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2021Article
- The potential role of COVID-19 in the induction of DNA damage.Mutation research. Reviews in mutation researchReview
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA polymerase delta (Pol δ) plays several essential roles in eukaryotic DNA replication and repair. At the replication fork, Pol δ is responsible for the synthesis and processing of the lagging-strand. At replication origins, Pol δ has been proposed to initiate leading-strand synthesis by extending the first Okazaki fragment. Destabilizing mutations in human Pol δ subunits cause replication stress and syndromic immunodeficiency. Analogously, reduced levels of Pol δ in Saccharomyces cerevisiae lead to pervasive genome instability. Here, we analyze how the depletion of Pol δ impacts replication origin firing and lagging-strand synthesis during replication elongation in vivo in S. cerevisiae. By analyzing nascent lagging-strand products, we observe a genome-wide change in both the establishment and progression of replication. S-phase progression is slowed in Pol δ depletion, with both globally reduced origin firing and slower replication progression. We find that no polymerase other than Pol δ is capable of synthesizing a substantial amount of lagging-strand DNA, even when Pol δ is severely limiting. We also characterize the impact of impaired lagging-strand synthesis on genome integrity and find increased ssDNA and DNA damage when Pol δ is limiting; these defects lead to a strict dependence on checkpoint signaling and resection-mediated repair pathways for cellular viability.
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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.