ArticleNature communications2025
The Fanconi anemia pathway repairs colibactin-induced DNA interstrand cross-links.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
8 citing papers in PubMed.
- Stage-Specific carcinogenic mechanisms and intervention strategies for pksArchives of microbiology · 2026Review
- Cellular effects of outer membrane vesicles isolated from pks-positive strains of bacteria.Research square · 2026Article
- 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
- Comprehensive review on Fanconi anemia: insights into DNA interstrand cross-links, repair pathways, and associated tumors.Orphanet journal of rare diseases · 2025Review
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Exploring the gut microbiome's role in colorectal cancer: diagnostic and prognostic implications.Frontiers in immunology · 2024Review
- Microbiota-derived small molecule genotoxins: host interactions and ecological impact in the gut ecosystem.Gut microbesReview
Corrections and comments
- Update of
Authors and funding
13 authors.
Funding
Abstract
Colibactin is a secondary metabolite produced by bacteria present in the human gut and is implicated in the development of colorectal cancer. This genotoxin alkylates deoxyadenosines on opposite strands of host cell DNA to produce DNA interstrand cross-links. While cells have evolved multiple mechanisms to resolve ("unhook") interstrand cross-links, little is known about which of these pathways promote resistance to colibactin. Here, we use Xenopus egg extracts to investigate replication-coupled repair of colibactin-induced interstrand cross-links. We show that replication fork stalling at a colibactin-induced interstrand cross-link activates the Fanconi anemia interstrand cross-link repair pathway, which unhooks the interstrand cross-link through nucleolytic incisions. These incisions generate a DNA double-strand break intermediate in one sister chromatid, which can be repaired by homologous recombination, and a monoadduct ("interstrand cross-link remnant") in the other. Translesion synthesis past the colibactin-induced interstrand cross-link remnant depends on Pol η and the Pol κ-REV1-Pol ζ polymerase complex and introduces predominantly T>A point mutations at the sites of colibactin alkylation. Taken together, our work provides a molecular framework for understanding how cells tolerate a naturally occurring and clinically relevant interstrand cross-link.
Indexed as
Identifiers
What OpenQuestion holds
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.