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Class switch recombination regulation by extracellular vesicles mediated intercellular epigenomic signaling

ABSTRACT: Class switch recombination regulation by extracellular vesicles mediated intercellular epigenomic signaling

PROVIDER: PRJNA1014428 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25960547.fastq.gz	Fastqsanger.gz
	SRR25960548.fastq.gz	Fastqsanger.gz
	SRR25960549.fastq.gz	Fastqsanger.gz
	SRR25960550.fastq.gz	Fastqsanger.gz
	SRR25960551.fastq.gz	Fastqsanger.gz

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Class switch recombination regulation by extracellular vesicles mediated intercellular epigenomic signaling

Project description:B cell maturation is crucial for effective adaptive immunity and requires a complex signaling network to control gene expression and protein function to mediate antibody diversification. B cells also rely on extracellular signaling queues from other cells within the germinal center. Recently, a novel class of intercellular signaling mediated by extracellular vesicles (EVs) has emerged. Studies have shown B cell EVs mediated signaling is involved in immune response regulation, infection control, and tumorigenesis. However, the mechanistic role of B cell EVs in B cell maturation is not yet established. We herein study the biological properties and physiological function of B cell EVs in the context of B cell maturation. We use novel technologies to characterize B cell EVs surface marker signatures, molecular cargo and physiological roles in B cell maturation. A new specialized nanoparticle analyzer was used to profile B cell EVs at the single particle level and characterize their surface markers and sub-populations at various maturation stages. EV ncRNA cargo was characterized by RNA-seq and bioinformatic analyses identified an EVs mediated regulatory network for B cell maturation. A previously uncharacterized micro-RNA (miR-5099) in combination with a set of long non-coding RNA carried within B cell EVs is shown to be important for antibody diversification signaling. The physiological role of EVs in B cell maturation is investigated using EV blockade assays and complementation studies using diverse EV sources further confirmed the physiological role and mode of action of EVs in B cell maturation.

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Lsh/HELLS is required for B lymphocyte development and immunoglobulin class switch recombination

Project description:We report here high-throughput sequencing analyses of class switch recombination junctions in Lsh deficient B cells with reduced capacity of class switch recombination compared to control B cells.

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Switch tandem repeats influence the choice of the alternative end-joining pathway in class switch recombination

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PTIP promotes chromatin changes critical for immunoglobulin class switch recombination

Project description:Programmed genetic rearrangements in lymphocytes require transcription at antigen receptor genes to promote accessibility for initiating double-strand break (DSB) formation critical for DNA recombination and repair. Here we show that activated B cells deficient in the PTIP component of the MLL3 (mixed-lineage leukemia 3) /MLL4 complex display impaired histone methylation (H3K4me3) and transcription initiation of downstream switch regions at the immunoglobulin heavy-chain (Igh) locus leading to defective immunoglobulin class-switching. We also show that PTIP accumulation at DSBs contributes to class-switch recombination (CSR) and genome stability independently from Igh switch transcription. These results demonstrate that PTIP promotes specific chromatin changes that control the accessibility of the Igh locus to CSR, and suggest a non-redundant role for the MLL3/MLL4 complex in altering antibody effector function. Genome-wide analysis of histone modifications, PTIP, and Pol II in PTIP-WT and PTIP-KO mouse activated B cells.

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PTIP promotes chromatin changes critical for immunoglobulin class switch recombination

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Senataxin and RNase H2 act redundantly to suppress genome instability during class switch recombination

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