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ABSTRACT: RNA-sequencing of S. cerevisiae with synthetic chromosome XI

PROVIDER: PRJNA1008435 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25753863_1.fastq.gz	Fastqsanger.gz
	SRR25753863_2.fastq.gz	Fastqsanger.gz
	SRR25753864_1.fastq.gz	Fastqsanger.gz
	SRR25753864_2.fastq.gz	Fastqsanger.gz
	SRR25753865_1.fastq.gz	Fastqsanger.gz

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Project description:X Chromosome Inactivation (XCI) is a female-specific process which balances X-linked gene dosage between sexes. Unstimulated T cells lack cytological enrichment of Xist RNA and heterochromatic modifications on the inactive X chromosome (Xi), and these modifications become enriched at the Xi after cell stimulation. Here, we examined allele-specific gene expression and epigenomic profiling of the Xi following T cell stimulation. We found that the Xi in unstimulated T cells is dosage compensated, and is enriched with the repressive H3K27me3 modification, but not H2AK119-ubiquitin (Ub) mark, including at promoters of XCI escape genes. Upon CD3/CD28 mediated T cell stimulation, the Xi accumulates H2AK119-Ub and H3K27me3 across the Xi. Next, we examined the T cell stimulation pathways responsible for Xist RNA localization to the Xi and found that T cell receptor (TCR) engagement, specifically NFkB signaling downstream of TCR, is required. Disruption of NFkB signaling, using inhibitors or genetic deletions, in mice and patients with immunodeficiencies prevents Xist/XIST RNA accumulation at the Xi and alters expression of some X-linked genes. Our findings reveal a novel connection between NFkB signaling pathways which impact XCI maintenance in female T cells.

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