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TCF1 dosage determines cell fate during T cell development.

ABSTRACT: TCF1 dosage determines cell fate during T cell development.

PROVIDER: PRJNA1152920 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR29442823_1.fastq.gz	Fastqsanger.gz
	SRR29442823_2.fastq.gz	Fastqsanger.gz
	SRR29442824_1.fastq.gz	Fastqsanger.gz
	SRR29442824_2.fastq.gz	Fastqsanger.gz

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TCF1 dosage determines cell fate during T cell development

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TCF1 dosage determines cell fate during T cell development

Project description:Loss of function studies have shown that transcription factor T cell factor-1 (TCF1), encoded by the Tcf7 gene, is essential for T cell development in the thymus. We discovered that the Tcf7 expression level is regulated by E box DNA binding proteins, independent of Notch, and regulates ab and gd T cell development. Systematic interrogation of the five E-protein binding elements (EPE1-5) in the Tcf7 enhancer region showed lineage-specific utilization. Specifically, loss-of-function analysis revealed that only EPE3 plays a critical role in supporting ab T cell development, while EPE1, 3 and 5 regulate gd T cell maturation and functional cell fate decision. The importance of EPE3 in supporting both lineages may stem from its unique capacity to interact with the Tcf7 transcriptional start site. Together these studies demonstrate that the precise dosage of TCF1 expression mediated by distinct EPEs generates a balanced output of T cells from the thymus.

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Transcription factor TCF1 binds Rorgt and orchestrates a regulatory network that determines homeostatic Th17 cell state [RNA-seq]

Project description:CD4+ T helper 17 (Th17) cells encompass a spectrum of cell states including homeostatic cells that maintain physiological functions such as barrier integrity and pathogenic cells that drive autoimmune tissue inflammation. Identifying the regulators that determine these cell states will provide means to control tissue inflammation without compromising the physiological functions of Th17 cells. Here, we identified TCF1 as the key regulator that determines Th17 cell state. IL-23, a cytokine critical for inducing pathogenic Th17 cells, decreased TCF1 expression. Consistent with this observation, conditional deletion of Tcf7/TCF1 in mature myelin-specific T cells conferred pathogenicity to homeostatic Th17 cells independent of IL-23. Conversely, sustained TCF1 expression impaired acquisition of pathogenicity. Integration of transcriptional and chromatin accessibility data showed that TCF1 maintained homeostatic state through a regulatory network involving ETS family transcription factors, EGR1, and FOXO1 and by binding to and interfering with RORt activity. Our findings provide mechanistic insight into how the homeostatic and pathogenic Th17 cell states are determined and into the association of genetic variants in TCF7 with susceptibility to autoimmunity.

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