{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Owen I"],"funding":["NINDS NIH HHS","National Institute of Neurological Diseases and Stroke","National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["jcs258578"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8445604"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["134(17)"],"pubmed_abstract":["Myxoid liposarcoma is caused by a chromosomal translocation resulting in a fusion protein comprised of the N terminus of FUS (fused in sarcoma) and the full-length transcription factor CHOP (CCAAT/enhancer-binding protein homologous protein, also known as DDIT3). FUS functions in RNA metabolism, and CHOP is a stress-induced transcription factor. The FUS-CHOP fusion protein causes unique gene expression and oncogenic transformation. Although it is clear that the FUS segment is required for oncogenic transformation, the mechanism of FUS-CHOP-induced transcriptional activation is unknown. Recently, some transcription factors and super enhancers have been proposed to undergo liquid-liquid phase separation and form membraneless compartments that recruit transcription machinery to gene promoters. Since phase separation of FUS depends on its N terminus, transcriptional activation by FUS-CHOP could result from the N terminus driving nuclear phase transitions. Here, we characterized FUS-CHOP in cells and in vitro, and observed novel phase-separating properties relative to unmodified CHOP. Our data indicate that FUS-CHOP forms phase-separated condensates that colocalize with BRD4, a marker of super enhancer condensates. We provide evidence that the FUS-CHOP phase transition is a novel oncogenic mechanism and potential therapeutic target for myxoid liposarcoma. This article has an associated First Person interview with the first author of the paper."],"journal":["Journal of cell science"],"pubmed_title":["The oncogenic transcription factor FUS-CHOP can undergo nuclear liquid-liquid phase separation."],"pmcid":["PMC8445604"],"funding_grant_id":["R35 GM119790","R01 NS116176","R35GM119790","R01NS116176","R01 GM118530"],"pubmed_authors":["Owen I","Wyne H","Fawzi NL","Yee D","Smyth J","Perdikari TM","Shewmaker F","Johnson V","Kortum R"],"additional_accession":[]},"is_claimable":false,"name":"The oncogenic transcription factor FUS-CHOP can undergo nuclear liquid-liquid phase separation.","description":"Myxoid liposarcoma is caused by a chromosomal translocation resulting in a fusion protein comprised of the N terminus of FUS (fused in sarcoma) and the full-length transcription factor CHOP (CCAAT/enhancer-binding protein homologous protein, also known as DDIT3). FUS functions in RNA metabolism, and CHOP is a stress-induced transcription factor. The FUS-CHOP fusion protein causes unique gene expression and oncogenic transformation. Although it is clear that the FUS segment is required for oncogenic transformation, the mechanism of FUS-CHOP-induced transcriptional activation is unknown. Recently, some transcription factors and super enhancers have been proposed to undergo liquid-liquid phase separation and form membraneless compartments that recruit transcription machinery to gene promoters. Since phase separation of FUS depends on its N terminus, transcriptional activation by FUS-CHOP could result from the N terminus driving nuclear phase transitions. Here, we characterized FUS-CHOP in cells and in vitro, and observed novel phase-separating properties relative to unmodified CHOP. Our data indicate that FUS-CHOP forms phase-separated condensates that colocalize with BRD4, a marker of super enhancer condensates. We provide evidence that the FUS-CHOP phase transition is a novel oncogenic mechanism and potential therapeutic target for myxoid liposarcoma. This article has an associated First Person interview with the first author of the paper.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2026-06-15T05:02:20.064Z","creation":"2025-04-06T03:30:25.832Z"},"accession":"S-EPMC8445604","cross_references":{"pubmed":["34357401"],"doi":["10.1242/jcs.258578"]}}