ArticleThe EMBO journal2015
Regulation of the Rev1-pol ζ complex during bypass of a DNA interstrand cross-link.
Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Treatment of Fanconi Anemia-Associated Head and Neck Cancer: Opportunities to Improve Outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Pooled it
- Mutagenic Potentials of DNA Interstrand Cross-Links Induced by 7,8-Dihydro-8-Oxoadenine.Molecules (Basel, Switzerland) · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- The Fanconi anemia pathway repairs colibactin-induced DNA interstrand cross-links.Nature communications · 2025Article
- ATM promotes reversed fork processing during DNA interstrand cross-link repair.bioRxiv : the preprint server for biology · 2025Article
- Leading and lagging strand abasic sites differentially affect vertebrate replisome progression but involve analogous bypass mechanisms.Nucleic acids research · 2025Article
- DNA polymerase kappa is the primary translesion synthesis polymerase for aldehyde ICLs.Nucleic acids research · 2025Article
- Comprehensive review on Fanconi anemia: insights into DNA interstrand cross-links, repair pathways, and associated tumors.Orphanet journal of rare diseases · 2025Review
- USP37 prevents premature disassembly of stressed replisomes by TRAIP.Nature communications · 2025Article
- FAN1-mediated translesion synthesis and POLQ/HELQ-mediated end joining generate interstrand crosslink-induced mutations.Nature communications · 2025Article
- Catalytic and noncatalytic functions of DNA polymerase κ in translesion DNA synthesis.Nature structural & molecular biology · 2025Article
- Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Molecular dependencies and genomic consequences of a global DNA damage tolerance defect.Genome biology · 2024Article
- Probing hot spots of protein-protein interactions mediated by the safety-belt region of REV7.Structure (London, England : 1993) · 2024Article
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- PARP1-dependent DNA-protein crosslink repair.Nature communications · 2024Article
- Article
- Control of DNA replication in vitro using a reversible replication barrier.Nature protocols · 2024Article
- Dual role of proliferating cell nuclear antigen monoubiquitination in facilitating Fanconi anemia-mediated interstrand crosslink repair.PNAS nexus · 2024Article
- Primordial germ cell DNA demethylation and development require DNA translesion synthesis.Nature communications · 2024Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
DNA interstrand cross-links (ICLs) are repaired in S phase by a complex, multistep mechanism involving translesion DNA polymerases. After replication forks collide with an ICL, the leading strand approaches to within one nucleotide of the ICL ("approach"), a nucleotide is inserted across from the unhooked lesion ("insertion"), and the leading strand is extended beyond the lesion ("extension"). How DNA polymerases bypass the ICL is incompletely understood. Here, we use repair of a site-specific ICL in Xenopus egg extracts to study the mechanism of lesion bypass. Deep sequencing of ICL repair products showed that the approach and extension steps are largely error-free. However, a short mutagenic tract is introduced in the vicinity of the lesion, with a maximum mutation frequency of ~1%. Our data further suggest that approach is performed by a replicative polymerase, while extension involves a complex of Rev1 and DNA polymerase ζ. Rev1-pol ζ recruitment requires the Fanconi anemia core complex but not FancI-FancD2. Our results begin to illuminate how lesion bypass is integrated with chromosomal DNA replication to limit ICL repair-associated mutagenesis.
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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.