ArticleNature communications2018
SUMO2 conjugation of PCNA facilitates chromatin remodeling to resolve transcription-replication conflicts.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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.
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Who cites it
37 citing papers in PubMed, 59 citations in OpenAlex.
- A Genetically Encoded Electrophilic Lysine Derivative Enables Sortase-Mediated Assembly of SUMO Activity-Based Probes.Journal of the American Chemical Society · 2026Article
- PCNA-RECQL5-RPRD1B recruit repair components to stressed replication forks to promote survival of BRCA1-deficient cancer cells.Nucleic acids research · 2026Article
- Sex-specific expression and function of TRIM28 during mouse primordial germ differentiation.iScience · 2025Article
- Distinct roles of RECQL5 in RAD51-mediated fork reversal and transcription elongation.Nucleic acids research · 2025Article
- Structural basis of RECQL5-induced RNA polymerase II transcription braking and subsequent reactivation.Nature structural & molecular biology · 2025Article
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- Clues to transcription/replication collision-induced DNA damage: it was RNAP, in the chromosome, with the fork.FEBS letters · 2025Review
- The role of SUMOylation in biomolecular condensate dynamics and protein localization.Cell insight · 2024Review
- ATM, KAP1 and the Epstein-Barr virus polymerase processivity factor direct traffic at the intersection of transcription and replication.Nucleic acids research · 2023Article
- The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023Review
- OTUD5 limits replication fork instability by organizing chromatin remodelers.Nucleic acids research · 2023Article
- RNAPII-dependent ATM signaling at collisions with replication forks.Nature communications · 2023Article
- Review
- SUMO Modification of Hepatitis B Virus Core Mediates Nuclear Entry, Promyelocytic Leukemia Nuclear Body Association, and Efficient Formation of Covalently Closed Circular DNA.Microbiology spectrum · 2023Article
- Human senataxin is a bona fide R-loop resolving enzyme and transcription termination factor.Nucleic acids research · 2023Article
- Fast friends - Ubiquitin-like modifiers as engineered fusion partners.Seminars in cell & developmental biology · 2022Review
- Uncover New Reactivity of Genetically Encoded Alkyl Bromide Non-Canonical Amino Acids.Frontiers in chemistry · 2022Article
- Bioinformatics-based analysis of SUMOylation-related genes in hepatocellular carcinoma reveals a role of upregulated SAE1 in promoting cell proliferation.Open medicine (Warsaw, Poland) · 2022Article
- Deorphanizing Caspase-3 and Caspase-9 Substrates In and Out of Apoptosis with Deep Substrate Profiling.ACS chemical biology · 2021Article
- Bromodomain proteins: protectors against endogenous DNA damage and facilitators of genome integrity.Experimental & molecular medicine · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
During DNA synthesis, DNA replication and transcription machinery can collide, and the replication fork may temporarily dislodge RNA polymerase II (RNAPII) to resolve the transcription-replication conflict (TRC), a major source of endogenous DNA double-strand breaks (DSBs) and common fragile site (CFS) instability. However, the mechanism of TRC resolution remains unclear. Here, we show that conjugation of SUMO2, but not SUMO1 or SUMO3, to the essential replication factor PCNA is induced on transcribed chromatin by the RNAPII-bound helicase RECQ5. Proteomic analysis reveals that SUMO2-PCNA enriches histone chaperones CAF1 and FACT in the replication complex via interactions with their SUMO-interacting motifs. SUMO2-PCNA enhances CAF1-dependent histone deposition, which correlates with increased histone H3.1 at CFSs and repressive histone marks in the chromatin to reduce chromatin accessibility. Hence, SUMO2-PCNA dislodges RNAPII at CFSs, and overexpressing either SUMO2-PCNA or CAF1 reduces the incidence of DSBs in TRC-prone RECQ5-deficient cells.
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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.