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Effects of TCF-1 de-repression on heterogeneity of chromatin states in memory and effector cells following acute infecton [scATAC-seq]

ABSTRACT: Effects of TCF-1 de-repression on heterogeneity of chromatin states in memory and effector cells following acute infecton [scATAC-seq]

PROVIDER: PRJNA1253759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR33239846_1.fastq.gz	Fastqsanger.gz
	SRR33239846_2.fastq.gz	Fastqsanger.gz
	SRR33239848_1.fastq.gz	Fastqsanger.gz
	SRR33239848_2.fastq.gz	Fastqsanger.gz

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Effects of TCF-1 de-repression on heterogeneity of chromatin states in memory and effector cells following acute infecton [scATAC-seq]

Project description:The transcription factor TCF-1 is downregulated during effector differentiation of CD8+ T cells. However, how its downregulation impacts epigenetic regulation of different effector- and memory-biased populations remains unclear. Here, we generate mice in which TCF-1 fails to become downregulated in differentiated effector cells and probe the epigenetic impact of TCF-1 retention on gene accessibiltiy patterns and moif enrichment patterns in CD8+ T cells on 8 dpi with LCMV-13 using scATAC-seq.

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Effects of TCF-1 de-repression on heterogeneity of effector and memory progenitor T cell transcriptomes in acute infection [scRNA-seq]

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Effects of TCF-1 de-repression on heterogeneity of effector and memory progenitor T cell transcriptomes in acute infection [scRNA-seq]

Project description:Effects of TCF-1 de-repression on heterogeneity of effector and memory progenitor T cell transcriptomes in acute infection [scRNA-seq]

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Intrinsically disordered domain of transcription factor TCF-1 is required for T cell developmental fidelity

Project description:In development, pioneer transcription factors access silent chromatin to reveal lineage-specific gene programs. The structured DNA-binding domains of pioneer factors have been well characterized, but whether and how low-complexity intrinsically disordered regions (IDRs) affect chromatin and control cell fate is unclear. Here, we report deletion of an IDR of the pioneer factor TCF-1, termed “L1”, leads to an early developmental block in T cells. The few T cells that develop from progenitors expressing TCF-1 lacking L1 exhibit lineage infidelity distinct from the lineage diversion of TCF-1 deficient cells. Mechanistically, L1 is required for activation of T cell genes and de-repression of GATA2 driven genes, normally reserved to the mast cell and dendritic cell lineages. Underlying this lineage diversion, L1 mediates binding of TCF-1 to its earliest target genes which are subject to repression as T cells develop. These data suggest TCF-1’s intrinsically disordered N-terminus maintains T cell lineage fidelity.

2024-06-16 | PXD043586 | Pride

scATAC-seq of mouse Plasmodium-specific CD4+ T cells

Project description:Plasmodium-specific CD4+ T cells from mice infected with Plasmodium chabaudi chabaudi AS parasites were recovered at Days 0, 4, 7, and 32 to undergo processing and to generate scATAC-seq dataset. At Day 7, CXCR5+ and CXCR6+ cells were recovered separately. At Day 32, mice were administered with either saline or artesunate (intermittent artesunate therapy - IAT). scATAC-seq dataset was analysed to investigate epigenomic landscapes of CD4+ T cells from effector to memory states.

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Liver X receptor controls follicular helper T cell differentiation via repression of TCF-1

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Effector differentiation downstream of lineage commitment in ILC1 is driven by Hobit across tissues.

Project description:Innate lymphoid cells (ILCs) mediate early immunity against infection and participate in tissue inflammation and homeostasis. It is unclear how ILCs acquire effector function, and whether these mechanisms differ between organs. Through multiplexed single-cell mRNA-sequencing we identified cKit+CD127hiTCF-1hi early differentiation stages of T-bet+ ILC1. These cells were present across different organs and had the potential to mature towards CD127intTCF-1int and CD127-TCF-1- ILC1. Paralleling a gradual loss of TCF-1, differentiating ILC1 forfeited their expansion potential while increasing expression of effector molecules, reminiscent of T cell differentiation in secondary lymphoid organs. The transcription factor Hobit was induced in TCF-1hi ILC1s and was required for their effector differentiation. These findings reveal sequential mechanisms of ILC1 lineage commitment and ILC1 effector differentiation that are conserved across tissues. Our analyses suggest that ILC1 emerge as TCF-1hi cells in the periphery and acquire a spectrum of organ-specific effector phenotypes through a uniform Hobit-dependent differentiation pathway driven by local cues.

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