ArticleThe Journal of biological chemistry2012
The Werner syndrome exonuclease facilitates DNA degradation and high fidelity DNA polymerization by human DNA polymerase δ.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- WRN exonuclease imparts high fidelity on translesion synthesis by Y family DNA polymerases.Genes & development · 2024Article
- Review
- Functional analysis ofAging · 2021Article
- Topoisomerase II contributes to DNA secondary structure-mediated double-stranded breaks.Nucleic acids research · 2020Article
- Epigenetic signatures of Werner syndrome occur early in life and are distinct from normal epigenetic aging processes.Aging cell · 2019Article
- Fidelity of DNA replication-a matter of proofreading.Current genetics · 2018Review
- RecQ and Fe-S helicases have unique roles in DNA metabolism dictated by their unwinding directionality, substrate specificity, and protein interactions.Biochemical Society transactions · 2018Review
- The Werner Syndrome Helicase Coordinates Sequential Strand Displacement and FEN1-Mediated Flap Cleavage during Polymerase δ Elongation.Molecular and cellular biology · 2017Article
- Strategic role of the ubiquitin-dependent segregase p97 (VCP or Cdc48) in DNA replication.Chromosoma · 2017Review
- Bloom's syndrome: Why not premature aging?: A comparison of the BLM and WRN helicases.Ageing research reviews · 2017Review
- Werner syndrome: Clinical features, pathogenesis and potential therapeutic interventions.Ageing research reviews · 2017Review
- Two Distinct Pathways Support Gene Correction by Single-Stranded Donors at DNA Nicks.Cell reports · 2016Article
- Article
- Review
- How Research on Human Progeroid and Antigeroid Syndromes Can Contribute to the Longevity Dividend Initiative.Cold Spring Harbor perspectives in medicine · 2016Review
- DNA secondary structure at chromosomal fragile sites in human disease.Current genomics · 2015Article
- Induction of action-at-a-distance mutagenesis by 8-oxo-7,8-dihydroguanine in DNA pol λ-knockdown cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2015Article
- Sphingosine, a modulator of human translesion DNA polymerase activity.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
DNA Polymerase δ (Pol δ) and the Werner syndrome protein, WRN, are involved in maintaining cellular genomic stability. Pol δ synthesizes the lagging strand during replication of genomic DNA and also functions in the synthesis steps of DNA repair and recombination. WRN is a member of the RecQ helicase family, loss of which results in the premature aging and cancer-prone disorder, Werner syndrome. Both Pol δ and WRN encode 3' → 5' DNA exonuclease activities. Pol δ exonuclease removes 3'-terminal mismatched nucleotides incorporated during replication to ensure high fidelity DNA synthesis. WRN exonuclease degrades DNA containing alternate secondary structures to prevent formation and enable resolution of stalled replication forks. We now observe that similarly to WRN, Pol δ degrades alternate DNA structures including bubbles, four-way junctions, and D-loops. Moreover, WRN and Pol δ form a complex with enhanced ability to hydrolyze these structures. We also present evidence that WRN can proofread for Pol δ; WRN excises 3'-terminal mismatches to enable primer extension by Pol δ. Consistent with our in vitro observations, we show that WRN contributes to the maintenance of DNA synthesis fidelity in vivo. Cells expressing limiting amounts (∼10% of normal) of WRN have elevated mutation frequencies compared with wild-type cells. Together, our data highlight the importance of WRN exonuclease activity and its cooperativity with Pol δ in preserving genome stability, which is compromised by the loss of WRN in Werner syndrome.
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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.