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

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

PROVIDER: PRJNA675570 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13010533_1.fastq.gz	Fastqsanger.gz
	SRR13010533_2.fastq.gz	Fastqsanger.gz
	SRR13010534_1.fastq.gz	Fastqsanger.gz
	SRR13010534_2.fastq.gz	Fastqsanger.gz
	SRR13010535_1.fastq.gz	Fastqsanger.gz

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

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

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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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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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Project description:The aberrant expansion of B1a cells has been observed in several murine autoimmune disease models; however, the mechanism of such proliferation of B1a cells is still limited. Here, we identify that Myb Like, SWIRM And MPN Domains 1 (MYSM1), a histone H2A deubiquitinase, plays an intrinsic role in the proliferation of B1a cells where MYSM1 deficiency results in the increased proliferation of B1a cells in mice. We demonstrate that MYSM1 recruits c-Myc to the promoter of miR-150 and stimulates the transcription of miR-150. Our further investigation shows that miR-150 decreases FMS-like tyrosine kinase 3 (FLT3) in B1a cells. In agreement with our animal studies, the percentage of FLT3+ B1 cells in Systemic Lupus Erythematosus (SLE) patients is significantly higher than healthy control. Thus, this study uncovers a novel pathway MYSM1/miR-150/FLT3 that inhibits proliferation of B1a, which may be involved in the pathogenesis of SLE.

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