ArticleNature structural & molecular biology2020
SLX4 interacts with RTEL1 to prevent transcription-mediated DNA replication perturbations.
Article in Nature structural & molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.
What it found
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Who cites it
30 citing papers in PubMed, 72 citations in OpenAlex.
- Phosphorylation by CDK1 switches the function of the human SLX4 SAP domain from DNA binding to MUS81 binding.Nucleic acids research · 2026Article
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription-replication conflicts.Nucleic acids research · 2026Article
- Review
- Rapid dynamics allow the low-abundance RTEL1 helicase to promote telomere replication.Nucleic acids research · 2025Article
- Structural and biochemical characterization of the C-terminal region of the human RTEL1 helicase.Protein science : a publication of the Protein Society · 2024Article
- A common mechanism for recruiting the Rrm3 and RTEL1 accessory helicases to the eukaryotic replisome.The EMBO journal · 2024Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- High expression of RTEL1 predicates worse progression in gliomas and promotes tumorigenesis through JNK/ELK1 cascade.BMC cancer · 2024Article
- Harmonin homology domain-mediated interaction of RTEL1 helicase with RPA and DNA provides insights into its recruitment to DNA repair sites.Nucleic acids research · 2024Article
- A comprehensive in silico investigation into the pathogenic SNPs in the RTEL1 gene and their biological consequences.PloS one · 2024Article
- Article
- OTUD5 limits replication fork instability by organizing chromatin remodelers.Nucleic acids research · 2023Article
- FAAP100 is required for the resolution of transcription-replication conflicts in primordial germ cells.BMC biology · 2023Article
- Comprehensive Interactome Mapping of the DNA Repair Scaffold SLX4 Using Proximity Labeling and Affinity Purification.Journal of proteome research · 2023Article
- Human senataxin is a bona fide R-loop resolving enzyme and transcription termination factor.Nucleic acids research · 2023Article
- Regulator of telomere elongation helicase 1 gene and its association with malignancy.Cancer reports (Hoboken, N.J.) · 2023Review
- FANCD2 promotes mitotic rescue from transcription-mediated replication stress in SETX-deficient cancer cells.Communications biology · 2022Article
- Changes in the architecture and abundance of replication intermediates delineate the chronology of DNA damage tolerance pathways at UV-stalled replication forks in human cells.Nucleic acids research · 2022Article
- SLX4 dampens MutSα-dependent mismatch repair.Nucleic acids research · 2022Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
22 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The SLX4 tumor suppressor is a scaffold that plays a pivotal role in several aspects of genome protection, including homologous recombination, interstrand DNA crosslink repair and the maintenance of common fragile sites and telomeres. Here, we unravel an unexpected direct interaction between SLX4 and the DNA helicase RTEL1, which, until now, were viewed as having independent and antagonistic functions. We identify cancer and Hoyeraal-Hreidarsson syndrome-associated mutations in SLX4 and RTEL1, respectively, that abolish SLX4-RTEL1 complex formation. We show that both proteins are recruited to nascent DNA, tightly co-localize with active RNA pol II, and that SLX4, in complex with RTEL1, promotes FANCD2/RNA pol II co-localization. Importantly, disrupting the SLX4-RTEL1 interaction leads to DNA replication defects in unstressed cells, which are rescued by inhibiting transcription. Our data demonstrate that SLX4 and RTEL1 interact to prevent replication-transcription conflicts and provide evidence that this is independent of the nuclease scaffold function of SLX4.
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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.