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Active maintenance of CD8+ T cell naïvety through regulation of global genome architecture [Hi-C]

ABSTRACT: Active maintenance of CD8+ T cell naïvety through regulation of global genome architecture [Hi-C]

PROVIDER: PRJNA937764 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23593352_1.fastq.gz	Fastqsanger.gz
	SRR23593352_2.fastq.gz	Fastqsanger.gz
	SRR23593353.fastq.gz	Fastqsanger.gz
	SRR23593354_1.fastq.gz	Fastqsanger.gz
	SRR23593354_2.fastq.gz	Fastqsanger.gz

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Active maintenance of CD8+ T cell naïvety through regulation of global genome architecture [Hi-C]

Project description:The differentiation of naïve CD8+ cytotoxic T lymphocytes (CTLs) into effector and memory states results in large scale changes in transcriptional and phenotypic profiles. Little is known about how large-scale changes in genome organisation reflect or underpin these transcriptional programs. We utilised Hi-C to map changes in the spatial organisation of long-range genome contacts within naïve, effector and memory virus-specific CD8+ T cells. We observed that the architecture of the naive CD8+ T cell genome was distinct from effector and memory genome configurations with extensive changes within discrete functional chromatin domains. However, deletion of the BACH2 or SATB1 transcription factors was sufficient to remodel the naïve chromatin architecture and engage transcriptional programs characteristic of differentiated cells. This suggests that the chromatin architecture within naïve CD8+ T cells is preconfigured to undergo autonomous remodelling upon activation, with key transcription factors restraining differentiation by actively enforcing the unique naïve chromatin state.

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Active maintenance of CD8+ T cell naïvety through regulation of global genome architecture

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Active maintenance of CD8+ T cell naïvety through regulation of global genome architecture [ATAC-seq]

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Active maintenance of CD8<sup>+</sup> T cell naivety through regulation of global genome architecture.

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Active maintenance of CD8<sup>+</sup> T cell naivety through regulation of global genome architecture.

Project description:The differentiation of naive CD8+ T lymphocytes into cytotoxic effector and memory CTL results in large-scale changes in transcriptional and phenotypic profiles. Little is known about how large-scale changes in genome organization underpin these transcriptional programs. We use Hi-C to map changes in the spatial organization of long-range genome contacts within naive, effector, and memory virus-specific CD8+ T cells. We observe that the architecture of the naive CD8+ T cell genome is distinct from effector and memory genome configurations, with extensive changes within discrete functional chromatin domains associated with effector/memory differentiation. Deletion of BACH2, or to a lesser extent, reducing SATB1 DNA binding, within naive CD8+ T cells results in a chromatin architecture more reminiscent of effector/memory states. This suggests that key transcription factors within naive CD8+ T cells act to restrain T cell differentiation by actively enforcing a unique naive chromatin state.

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Project description:Eukaryotic genome spatial folding plays a key role in genome function. Decoding the principles and dynamics of 3D genome organization depends on improving technologies to achieve higher resolution. Chromatin domains have been suggested as regulatory micro-environments, whose identification is crucial to understand the genome architecture. We report here that our recently developed method, Hi-TrAC, which specializes in detecting chromatin loops among genomic accessible regulatory regions, allows us to examine active domains with limited sequencing depths at a high resolution. Hi-TrAC can detect active sub-TADs with a median size of 100kb, most of which harbor one or two cell specifically expressed genes and regulatory elements such as super-enhancers organized into nested interaction domains. These active sub-TADs are characterized by highly enriched signals of histone mark H3K4me1 and chromatin-binding proteins, including Cohesin complex. We show that knocking down core subunit of the Cohesin complex using shRNAs in human cells or decreasing the H3K4me1 modification by deleting the H3K4 methyltransferase Mll4 gene in mouse Th17 cells disrupted the sub-TADs structure. In summary, Hi-TrAC serves as a compatible and highly responsive approach to studying dynamic changes of active sub-TADs, allowing us more explicit insights into delicate genome structures and functions.

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Active maintenance of CD8+ T cell naïvety through regulation of global genome architecture

Project description:This SuperSeries is composed of the SubSeries listed below.

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