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Gene expression profiling in RagC T89N germinal center B cells and RagC S74C murine B220+ lymphoma cells

ABSTRACT: Gene expression profiling in RagC T89N germinal center B cells and RagC S74C murine B220+ lymphoma cells

PROVIDER: PRJNA516208 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8467580.fastq.gz	Fastqsanger.gz
	SRR8467590.fastq.gz	Fastqsanger.gz
	SRR8467581.fastq.gz	Fastqsanger.gz
	SRR8467591.fastq.gz	Fastqsanger.gz
	SRR8467582.fastq.gz	Fastqsanger.gz

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Gene expression profiling in RagC T89N germinal center B cells and RagC S74C murine B220+ lymphoma cells

Project description:Gene expression by RNAseq in murine germinal centers induced by SRBC in RagC T89N mice (YRT codes) and RNAseq in murine B220+ from VavVPBcl2/RagC S74C and VavVPBcl2/RagC +/+ lymphomas Follicular Lymphoma (FL) is an incurable B cell malignancy derived from germinal center (GC) B cells. The RRAGC gene, encoding a GTPase that links cellular nutrient sufficiency with the activation of mechanistic target of rapamycin complex 1 (mTORC1) is mutated in 15% of FL patients, but its impact in B cell functions and lymphomas is unexplored. Endogenous expression of Rragc mutant variants in B lymphocytes from novel knock-in strains of mice resulted in a partial insensitivity of mTORC1 to nutrient deprivation. A mild, but not a full-blown activation of the nutrient signaling pathway enhanced B cell activation and the GC response, suppressed apoptosis, and accelerated lymphomagenesis. Moreover, murine RRAGC mutant FL showed selective vulnerability to pharmacological inhibition of mTORC1. This moderate increase in nutrient signaling synergized with paracrine cues from the supportive T cell microenvironment that activate mTORC1 via the PI3K-Akt axis to promote B cell activation. Hence, RRAGC mutations sustained experimental GCs and murine and human FL in the presence of decreased T cell support. Moreover, mutations in RRAGC in human FLs are mutually-exclusive with mutations that result in increased abundance of T helper cells, consistent with functional redundancy between those pathways. Taken together, our results support a model in which activating mutations in the nutrient signaling pathway foster lymphomagenesis by corrupting a nutrient-dependent control of mTORC1-activating paracrine signals from the T cell microenvironment

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Gene expression profiling in RagC Q119L murine B220+ lymphoma cells

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Gene expression profiling in RagC Q119L murine germinal centre B cells and B220+ lymphoma cells

Project description:Gene expression profiling in RagC Q119L murine germinal centre B cells and B220+ lymphoma cells

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Gene expression profiling in RagC S74C germinal center B cells

Project description:Gene expression profiling in RagC S74C germinal center B cells

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Gene expression profiling in RagC Q119L germinal centre B cells

Project description:Gene expression by RNAseq in murine RagC Q119L/+ and RagC +/+ germinal centre B cells

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Gene expression profiling in RagC Q119L murine B220+ lymphoma cells

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Gene expression profiling in RagC S74C germinal center B cells

Project description:Gene expression by RNAseq in murine germinal center B cells induced by SRBC in RagC S74C mice Follicular Lymphoma (FL) is an incurable B cell malignancy derived from germinal center (GC) B cells. The RRAGC gene, encoding a GTPase that links cellular nutrient sufficiency with the activation of mechanistic target of rapamycin complex 1 (mTORC1) is mutated in 15% of FL patients, but its impact in B cell functions and lymphomas is unexplored. Endogenous expression of Rragc mutant variants in B lymphocytes from novel knock-in strains of mice resulted in a partial insensitivity of mTORC1 to nutrient deprivation. A mild, but not a full-blown activation of the nutrient signaling pathway enhanced B cell activation and the GC response, suppressed apoptosis, and accelerated lymphomagenesis. Moreover, murine RRAGC mutant FL showed selective vulnerability to pharmacological inhibition of mTORC1. This moderate increase in nutrient signaling synergized with paracrine cues from the supportive T cell microenvironment that activate mTORC1 via the PI3K-Akt axis to promote B cell activation. Hence, RRAGC mutations sustained experimental GCs and murine and human FL in the presence of decreased T cell support. Moreover, mutations in RRAGC in human FLs are mutually-exclusive with mutations that result in increased abundance of T helper cells, consistent with functional redundancy between those pathways. Taken together, our results support a model in which activating mutations in the nutrient signaling pathway foster lymphomagenesis by corrupting a nutrient-dependent control of mTORC1-activating paracrine signals from the T cell microenvironment

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ChIPseq analyses in germinal center B cells

Project description:Germinal center B cells were isolated from human tonsil tissue and crosslinked. ChIP was performed on two distinct pools of germinal center cells, each obtained from 3-5 donors. The experiment includes two biological replicates (germinal center cell pools from different donors). ChIP was performed on both pools and subject to library preparation and sequencing. Input DNA was sequenced for both pools.

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