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ABSTRACT: Multi-omics study of DBD-a4 helix of EWS::FLI in TTC466 cells

PROVIDER: PRJNA1116744 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR29198400_1.fastq.gz	Fastqsanger.gz
	SRR29198400_2.fastq.gz	Fastqsanger.gz
	SRR29198401_1.fastq.gz	Fastqsanger.gz
	SRR29198401_2.fastq.gz	Fastqsanger.gz

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EWS::FLI cooperatively binds at GGAA microsatellites via DBD-a4 helix

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Project description:Using EWS-FLI and its parental transcription factor, FLI1, we created a unique experimental system to address questions regarding the genomic mechanisms by which chimeric transcription factors cause cancer. We found that in tumor cells, EWS-FLI targets regions of the genome distinct from FLI1, despite identical DNA-binding domains. In primary endothelial cells, however, EWS-FLI and FLI1 demonstrate similar targeting. To understand this mistargeting, we examined chromatin organization. Regions targeted by EWS-FLI are normally repressed and nucleosomal in primary endothelial cells. In tumor cells, however, bound regions are nucleosome-depleted and harbor the chromatin signature of enhancers. We next demonstrated that through chimerism, EWS-FLI acquired the ability to alter chromatin. Expression of EWS-FLI results in nucleosome depletion at targeted sites, whereas silencing of EWS-FLI in tumor cells restored nucleosome occupancy. Thus, the EWS-FLI chimera acquired chromatin-altering activity, leading to mistargeting, chromatin disruption, and ultimately transcriptional dysregulation. Examination of two transcription factors in two different cell types, as well as three histone methylation marks and FAIRE

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