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An RFX/miR-150 axis restrains proliferation of primary human T lymphocytes

ABSTRACT: An RFX/miR-150 axis restrains proliferation of primary human T lymphocytes

PROVIDER: PRJNA675555 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13010505_1.fastq.gz	Fastqsanger.gz
	SRR13010505_2.fastq.gz	Fastqsanger.gz
	SRR13010506_1.fastq.gz	Fastqsanger.gz
	SRR13010506_2.fastq.gz	Fastqsanger.gz
	SRR13010507_1.fastq.gz	Fastqsanger.gz

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An RFX/miR-150 axis regulates proliferation of primary human T lymphocytes

Project description:An RFX/miR-150 axis regulates proliferation of primary human T lymphocytes

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An RFX/miR-150 axis restrains proliferation of primary human T lymphocytes

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RFX transcription factors control a miR-150/PDAP1 axis that restrains the proliferation of human T cells.

Project description:Within the immune system, microRNAs (miRNAs) exert key regulatory functions. However, what are the mRNA targets regulated by miRNAs and how miRNAs are transcriptionally regulated themselves remain for the most part unknown. We found that in primary human memory T helper lymphocytes, miR-150 was the most abundantly expressed miRNA, and its expression decreased drastically upon activation, suggesting regulatory roles. Constitutive MIR150 gene expression required the RFX family of transcription factors, and its activation-induced down-regulation was linked to their reduced expression. By performing miRNA pull-down and sequencing experiments, we identified PDGFA-associated protein 1 (PDAP1) as one main target of miR-150 in human T lymphocytes. PDAP1 acted as an RNA-binding protein (RBP), and its CRISPR/Cas-9-mediated deletion revealed that it prominently contributed to the regulation of T-cell proliferation. Overall, using an integrated approach involving quantitative analysis, unbiased genomics, and genome editing, we identified RFX factors, miR-150, and the PDAP1 RBP as the components of a regulatory axis that restrains proliferation of primary human T lymphocytes.

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An RFX/miR-150 axis regulates proliferation of primary human T lymphocytes

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miR-150 Pulldown-sequencing data

Project description:miR-150 Pulldown-sequencing data

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Project description:Human CD4+ Total memory cells (CD4+CD25-CD45RA-CCR7+/-) were activated for 5d with anti-CD3/anti-CD28 antibodies and transfected with biotinylated miR-150 mimic or biotinylated mimic negative control by Exiqon. After 24h cells were lysed and miRNA:mRNA complexes pulled-down with streptavidin agarose O/N at 4°C. RNA was then purified using TRI-reagent and RNA zymospin columns. Three independent donors were used for this experiment. Inputs were also sequenced. Total RNA was sequenced in single end mode. This experiment is assessing direct targets bound by miR-150-5p in human T cells.

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Project description:MicroRNAs are a major class of gene regulators in mammals. While numerous aspects of the immune systems are controlled by miRNAs, their precise role in the CD8+ T cell response remains unclear. In this report, we show that miR-150 is the most abundant miRNA expressed in CD8+ T cells and its expression is required for proper effector cell differentiation in response to acute and chronic pathogens. In the absence of miR-150, CD8+ T cells failed to both undergo robust expansion and differentiate into short-lived terminal effector cells. The lack of miR-150 also altered the effector CD8+ T cell transcriptome such that, despite activation, genes associated with naïve or memory cells were highly expressed. The deletion of miR-150 also reduced killing efficiency of CD8+ T cells. These results uncover a cell-intrinsic role for miR-150 in the regulation of CD8+ T cell effector fate and function.

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