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SS18::SSX redistributes BAF chromatin remodelers selectively to activate and repress transcription [scRNA-Seq]

ABSTRACT: SS18::SSX redistributes BAF chromatin remodelers selectively to activate and repress transcription [scRNA-Seq]

PROVIDER: PRJNA1123666 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR29398045.fastq.gz	Fastqsanger.gz
	SRR29398046.fastq.gz	Fastqsanger.gz
	SRR29398047.fastq.gz	Fastqsanger.gz
	SRR29398048.fastq.gz	Fastqsanger.gz

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SS18::SSX redistributes BAF chromatin remodelers selectively to activate and repress transcription [RNA-Seq]

Project description:SS18::SSX redistributes BAF chromatin remodelers selectively to activate and repress transcription [RNA-Seq]

| PRJNA1123667 | ENA

SS18::SSX redistributes BAF chromatin remodelers selectively to activate and repress transcription [ChIP-Seq, Hi-ChIP]

Project description:SS18::SSX redistributes BAF chromatin remodelers selectively to activate and repress transcription [ChIP-Seq, Hi-ChIP]

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SS18::SSX redistributes BAF chromatin remodelers selectively to activate and repress transcription [ChIP-Seq, Hi-ChIP]

Project description:In order to evaluate SS18::SSX distribution across chromatin in synovial sarcoma, we performed ChIP-seq from mouse SyS tumors expressing the human SS18::SSX2 using an antibody specific for the fusion oncoprotein SS18::SS. ChIP-seq was also employed to assess SyS genome profiles of specific chromatin histone marks (H2AK119ub, H3K4me1, H3K4me3, H3K27ac and H3K27me3), and chromatin conformation by HiChIP was evaluated using an antibody against H3K27ac to identify enhancer loops for the purpose of assigning distal regulatory elements to specific genes. Furthermore, we also characterize the distribution of each BAF family subtypes with ChIP-seq ( ARID1A (cBAF), DPF2 (cBAF), PBRM1 (PBAF) and BRD9 (GBAF/non-canonical BAF)). In this study, our fundings suggest that SS18::SSX distributes to proximal and distal regulatory elements bearing ubiquitylated histone 2A and GBAF distributes with the fusion to broad proximal and distal regions; CBAF and PBAF distribute narrowly to active transcriptional start sites.

2025-06-10 | GSE269770 | GEO

SS18::SSX redistributes BAF chromatin remodelers selectively to activate and repress transcription [RNA-Seq]

Project description:Synovial sarcoma (SS) is a rare malignancy, involves a t(X;18) chromosomal translocation that creates a fusion gene SS18-SSX. SS18 is a chromatin remodeling BAF-complexes component, which incorporated in CBAF and GBAF (non-canonical ncBAF). Our previous studies determined that incorporation of the fusion oncoprotein caused degradation of CBAF complexes, emphasizing a critical oncogenic function of GBAF and PBAF in synovial sarcomagenesis. To determine the SyS dependencies on different subtypes of BAF complexes during tumor development in vivo, we used our SyS mouse model combined with genetic disruption of specific BAF complexes components ARID1A/B or PBRM1. In this study, our fundings suggest that depletion of ARID1A and ARID1B sped tumorigenesis, without significant change in the histomorphology of the developing tumors. Loss of PBRM1 also led to faster tumor growing, but Pbrm1-silenced tumors lacked the full array of SyS histomorphologies observed in wildtype tumors. Overall, Arid1a or Arid1b disruption rendered tumor transcriptomes that clustered within the hSS2 tumor transcriptomes, unlike Pbrm1 disrupted tumors.

2025-06-10 | GSE269772 | GEO

A stage-specific induction system reveals that the oncogenic fusion protein in synovial sarcoma, SS18-SSX, is a cellular context-dependent epigenetic modifier

Project description:We analyzed the effects of cellular context on the function of the synovial sarcoma-specific fusion protein, SS18-SSX, using human pluripotent stem cells containing the drug-inducible SS18-SSX gene. To investigate the cell-type-dependent effecfts of SS18-SSX, we performed gene expression profiling experiments. Comparison of global gene expressions of hPSCs, hPSC-NCCs, and hPSC-MSCs with or without the inductuion of SS18-SSX2

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The SS18-SSX fusion oncoprotein hijacks BAF complex targeting and function to drive synovial sarcoma [ATAC-seq]

Project description:Synovial sarcoma (SS) is defined by the hallmark SS18-SSX fusion oncoprotein, which renders BAF complexes aberrant in two manners: gain of SSX to the SS18 subunit and concomitant loss of BAF47 subunit assembly. Here we demonstrate that SS18-SSX globally hijacks BAF complexes on chromatin to activate a SS transcriptional signature we define using primary tumors and cell lines. Specifically, SS18-SSX retargets BAF complexes from enhancers to broad polycomb domains to oppose PRC2-mediated repression and activate bivalent genes. Upon suppression of SS18-SSX, reassembly of BAF47 restores enhancer activation, but is not required for proliferative arrest. These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.

2018-05-31 | GSE114487 | GEO

The SS18-SSX fusion oncoprotein hijacks BAF complex targeting and function to drive synovial sarcoma [ChIP-Seq]

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The SS18-SSX fusion oncoprotein hijacks BAF complex targeting and function to drive synovial sarcoma [RNA-Seq Tumor]

2018-05-31 | GSE108027 | GEO

The SS18-SSX fusion oncoprotein hijacks BAF complex targeting and function to drive synovial sarcoma [RNA-Seq Cell]

2018-05-31 | GSE108026 | GEO

The SS18-SSX oncoprotein hijacks KDM2B-PRC1.1 to drive synovial sarcoma [ChIP-seq]

Project description:Gene fusions arising from chromosomal translocations are key oncogenic drivers in soft tissue sarcomas but little is known about how they exert their oncogenic effects. Our study explores the molecular mechanisms by which the SS18-SSX fusion oncoprotein subverts epigenetic mechanisms of gene regulation to drive synovial sarcoma. Using functional genomics, we identify KDM2B – a histone demethylase and core component of a non-canonical Polycomb Repressive Complex 1 (PRC1.1) – as selectively required for sustaining synovial sarcoma cell transformation. SS18-SSX physically interacts with PRC1.1 and co-associates with SWI/SNF and KDM2B complexes on unmethylated CpG islands genome-wide. Via KDM2B, SS18-SSX binds and aberrantly activates expression of a series of developmentally regulated transcription factors that would otherwise be targets of polycomb-mediated repression, which is restored upon KDM2B depletion leading to irreversible mesenchymal differentiation. Thus, SS18-SSX de-regulates developmental programs to drive transformation by hijacking a transcriptional repressive complex to aberrantly activate gene expression.

2018-03-01 | GSE108926 | GEO

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