ArticleThe Journal of biological chemistry2022
Stable G-quadruplex DNA structures promote replication-dependent genome instability.
Article in The Journal of biological chemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- G-quadruplex structures as regulators of cellular processes and drivers of genome instability in cancer.Critical reviews in biochemistry and molecular biology · 2026Review
- G-quadruplex homeostasis is a determinant of PARP inhibitor toxicity in BRCA2-deficient cells.Nature communications · 2026Article
- The G-force in the genome: Unknowns on the functional flairs of DNA G-quadruplexes.PLoS biology · 2026Article
- Human REV1 interacts with DHX36 to promote replication and tolerance of G-quadruplex DNA.Nucleic acids research · 2026Article
- Canonical and noncanonical forms of G4 DNA at cluster III of the BCL6 breakpoint region could lead to chromosomal translocation in DLBCL.The Journal of biological chemistry · 2026Article
- The SMARCA4 subunit of the SWI/SNF complex prevents genome instability at G quadruplexes.Genome biology · 2026Article
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- Non-B DNA structures and their contributions to genetic diversity, aging, and disease.Nucleic acids research · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- G4STAB: a multi-input deep learning model to predict G-quadruplex thermodynamic stability based on sequence and salt concentration.Bioinformatics (Oxford, England) · 2025Article
- Mutations and Recombination at G4 DNA-Forming Sequences Exacerbated by CPT-Resistant Mutant Topoisomerase 1 Is Dependent on SUMOylation.International journal of molecular sciences · 2025Article
- Human TLS DNA polymerase: saviors or threats under replication stress?Molecular and cellular biochemistry · 2025Review
- The effect of prolonged G-quadruplex stabilization on the functions of human cells.Scientific reports · 2025Article
- G-quadruplex-stalled eukaryotic replisome structure reveals helical inchworm DNA translocation.Science (New York, N.Y.) · 2025Article
- Elevated reactive oxygen species can drive the alternative lengthening of telomeres pathway in ATRX-null cancers.Nucleic acids research · 2025Article
- G-quadruplex stabilization provokes DNA breaks in human PKD1, revealing a second hit mechanism for ADPKD.Nature communications · 2025Article
- Triplex H-DNA structure: the long and winding road from the discovery to its role in human disease.NAR molecular medicine · 2024Article
- Stressed? Break-induced replication comes to the rescue!DNA repair · 2024Review
- Structural Unfolding of G-Quadruplexes: From Small Molecules to Antisense Strategies.Molecules (Basel, Switzerland) · 2024Review
- Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.NAR cancer · 2024Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
G-quadruplex (G4)-prone structures are abundant in mammalian genomes, where they have been shown to influence DNA replication, transcription, and genome stability. In this article, we constructed cells with a single ectopic homopurine/homopyrimidine repeat tract derived from the polycystic kidney disease type 1 (PKD1) locus, which is capable of forming triplex (H3) and G4 DNA structures. We show that ligand stabilization of these G4 structures results in deletions of the G4 consensus sequence, as well as kilobase deletions spanning the G4 and ectopic sites. Furthermore, we show that DNA double-strand breaks at the ectopic site are dependent on the nuclease Mus81. Hypermutagenesis during sister chromatid repair extends several kilobases from the G4 site and breaks at the G4 site resulting in microhomology-mediated translocations. To determine whether H3 or G4 structures are responsible for homopurine/homopyrimidine tract instability, we derived constructs and cell lines from the PKD1 repeat, which can only form H3 or G4 structures. Under normal growth conditions, we found that G4 cell lines lost the G4 consensus sequence early during clonal outgrowth, whereas H3 cells showed DNA instability early during outgrowth but only lost reporter gene expression after prolonged growth. Thus, both the H3 and G4 non-B conformation DNAs exhibit genomic instability, but they respond differently to endogenous replication stress. Our results show that the outcomes of replication-dependent double-strand breaks at non-B-DNAs model the instability observed in microhomology-mediated break-induced replication (BIR). Marked variability in the frequency of mutagenesis during BIR suggests possible dynamic heterogeneity in the BIR replisome.
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