ArticleProtein science : a publication of the Protein Society2021
FUS oncofusion protein condensates recruit mSWI/SNF chromatin remodeler via heterotypic interactions between prion-like domains.
Article in Protein science : a publication of the Protein Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- How do low-complexity domain interactions control transcription?Biochemical Society transactions · 2026Review
- Condensates in fusion oncoprotein-driven leukemia: new biology and therapeutic opportunities.Trends in cancer · 2026Review
- Amyloid-β, Tau Protein, α-Synuclein, TDP-43, and FUS in Mixed Pathology: And Intrinsic Disorder to Rule Them All.International journal of molecular sciences · 2026Review
- FUS nanoclusters are a distinct state within the dilute phase.Nature communications · 2025Article
- Deciphering the molecular mechanisms of FET fusion oncoprotein-DNA hollow co-condensates.Nature communications · 2025Article
- Chromatin Binding Regulates Phase Behavior and Morphology of Condensates Formed by Prion-like Domains.Journal of molecular biology · 2025Article
- Condensation-dependent interactome of a chromatin remodeler underlies tumor suppressor activities.Nature communications · 2025Article
- Phase-separating fusion proteins drive cancer by upsetting transcription regulation.Genome biology · 2025Article
- FET fusion oncoproteins enrich SWI/SNF complex subtypes and interaction partners.Cellular & molecular biology letters · 2025Article
- Biomolecular phase separation in tumorigenesis: from aberrant condensates to therapeutic vulnerabilities.Molecular cancer · 2025Review
- Large-scale discovery of chromatin dysregulation induced by oncofusions and other protein-coding variants.Nature biotechnology · 2025Article
- Phase Separation in Chromatin Organization and Human Diseases.International journal of molecular sciences · 2025Review
- TFE3 fusion oncoprotein condensates drive transcriptional reprogramming and cancer progression in translocation renal cell carcinoma.Cell reports · 2025Article
- Hijacking the BAF complex: the mechanistic interplay of ARID1A and EWS::FLI1 in Ewing sarcoma.Molecular oncology · 2025Article
- Transcription regulation by biomolecular condensates.Nature reviews. Molecular cell biology · 2025Review
- FUS::DDIT3 Fusion Protein in the Development of Myxoid Liposarcoma and Possible Implications for Therapy.Biomolecules · 2024Review
- Direct computations of viscoelastic moduli of biomolecular condensates.The Journal of chemical physics · 2024Article
- Liquid-liquid phase separation in diseases.MedComm · 2024Review
- Determinants that enable disordered protein assembly into discrete condensed phases.Nature chemistry · 2024Article
- Phase separation and transcriptional regulation in cancer development.Journal of biomedical research · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Fusion transcription factors generated by genomic translocations are common drivers of several types of cancers including sarcomas and leukemias. Oncofusions of the FET (FUS, EWSR1, and TAF15) family proteins result from the fusion of the prion-like domain (PLD) of FET proteins to the DNA-binding domain (DBD) of certain transcription regulators and are implicated in aberrant transcriptional programs through interactions with chromatin remodelers. Here, we show that FUS-DDIT3, a FET oncofusion protein, undergoes PLD-mediated phase separation into liquid-like condensates. Nuclear FUS-DDIT3 condensates can recruit essential components of the global transcriptional machinery such as the chromatin remodeler SWI/SNF. The recruitment of mammalian SWI/SNF (mSWI/SNF) is driven by heterotypic PLD-PLD interactions between FUS-DDIT3 and core subunits of SWI/SNF, such as the catalytic component BRG1. Further experiments with single-molecule correlative force-fluorescence microscopy support a model wherein the fusion protein forms condensates on DNA surface and enrich BRG1 to activate transcription by ectopic chromatin remodeling. Similar PLD-driven co-condensation of mSWI/SNF with transcription factors can be employed by other oncogenic fusion proteins with a generic PLD-DBD domain architecture for global transcriptional reprogramming.
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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.