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RNA-seq analysis after overexpression of miR-148a in keratinocytes

ABSTRACT: RNA-seq analysis after overexpression of miR-148a in keratinocytes

PROVIDER: PRJNA812523 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18212878_1.fastq.gz	Fastqsanger.gz
	SRR18212878_2.fastq.gz	Fastqsanger.gz
	SRR18212879_1.fastq.gz	Fastqsanger.gz
	SRR18212879_2.fastq.gz	Fastqsanger.gz
	SRR18212880_1.fastq.gz	Fastqsanger.gz

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RNA-seq analysis after overexpression of miR-148a in keratinocytes

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miR-148a controls metabolic programming and survival of mature CD19-negative plasma cells

Project description:Long-lived antibody-secreting plasma cells are essential to establish humoral memory against pathogens. While a plasma cell gene signature has been established, elaborate key regulators remain enigmatic.The plasma cell signature microRNA miR-148a favors in vitro differentiation of plasmablasts by repressing the germinal center transcription factor Bach2 and pro-apoptotic BIM and PTEN. To determine whether miR-148a fine-tunescontrols the in vivo development of B cells into long-lived plasma cells, we established mice with a genomic, conditional and inducible deletion of miR-148a. The analysis of miR-148a-deficient mice revealed reduced serum Ig, decreased numbers of newly formed plasmablasts and a reduced CD19-negative, CD93-positive long-lived plasma cells compartment. RNASeq and metabolic analysis showed an impaired glucose uptake and oxidative phosphorylation-based energy metabolism, altered abundance of homing receptors CXCR3 (increase) and CXCR4 (reduction) in miR-148a-deficient plasma cells. These findings establish the importance of miR-148a as a regulator of the differentiation and maintenance of late CD19-negative mature plasma cells by controlling their metabolism and retention in the bone marrow niche. clearly undermine our model of miR-148a as a regulator of the maintenance of long-lived plasma cells.

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