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Tumor transcriptomes profiling of SS18-SSX, Smarcb1-/- and combination of SS18-SSX and Smarcb1-/- driven tumor

ABSTRACT: Tumor transcriptomes profiling of SS18-SSX, Smarcb1-/- and combination of SS18-SSX and Smarcb1-/- driven tumor

PROVIDER: PRJNA644360 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12153514_1.fastq.gz	Fastqsanger.gz
	SRR12153514_2.fastq.gz	Fastqsanger.gz
	SRR12153515_1.fastq.gz	Fastqsanger.gz
	SRR12153515_2.fastq.gz	Fastqsanger.gz
	SRR12153516_1.fastq.gz	Fastqsanger.gz

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Tumor transcriptomes profiling of SS18-SSX, Smarcb1-/- and combination of SS18-SSX and Smarcb1-/- driven tumor

Project description:We generated mouse tumors of each combination of genotypes that included either presence or absence of heterozygosity for hSS2 in Rosa26 and homozygosity for wildtype or floxed alleles of Smarcb1. In order to test how these different tumor genotypes impacted BAF distribution across the genome, we performed ChIPseq in tumors of each genotype for member components shared by all BAF subtypes, SMARCC1 (also named BAF155) and SMARCA4 (also named BRG1.) We also performed ChIPseq for RNAPOLII to determine the BAF relationship with transcription in each genotype. The length of peaks is extended in fusion-expressing tumors, regardless of Smarcb1 status. The heatmaps of SMARCC1 enrichments at transcription start sites (TSSs) across the genome in fusion-only tumors demonstrate a very similar overall pattern with that in combination genotype tumors, which suggested that the fusion plays a deterministic role in the distribution of BAF complexes across the genome. Specifically around each TSS across the genome was a striking absence of BAF enrichment in both groups that bore genetic silencing of Smarcb1, not present in the fusion-only group. This suggests that some SMARCB1-retaining BAF complex is necessary to permit binding to the TSS or the +1 nucleosome position. Fusion expression and Smarcb1 silencing have different impacts on BAF genomic locations.

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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.

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