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MRNA-seq of wild-type or p53-deficient B cells expressing MHV68 M2

ABSTRACT: mRNA-seq of wild-type or p53-deficient B cells expressing MHV68 M2

PROVIDER: PRJNA936439 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23517700.fastq.gz	Fastqsanger.gz
	SRR23517701.fastq.gz	Fastqsanger.gz
	SRR23517702.fastq.gz	Fastqsanger.gz
	SRR23517703.fastq.gz	Fastqsanger.gz
	SRR23517704.fastq.gz	Fastqsanger.gz

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mRNA-seq of wild-type or p53-deficient B cells expressing MHV68 M2

Project description:Gammaherpesviruses (GHV) are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus (EBV) and murine gammaherpesvirus 68 (MHV68), this is accomplished through a viral gene-expression program that promotes cellular proliferation and differentiation, especially of germinal center (GC) B cells. Intrinsic host mechanisms to control virus-driven cellular expansion are incompletely defined. Using a small-animal model of GHV pathogenesis, we identify the B cell-specific latency gene M2, an MHV68 mediator of GC B cell differentiation, as a viral gene product that is sufficient to induce p53 in a manner that is dependent on Src kinase activity. To understand the function of M2 in primary B cells, we performed retroviral transduction of M2 or M2.Stop in wild-type or p53-deficient B cells. Our results reveal p53 and cellular proliferation pathways enriched in M2-expressing B cells.

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mRNA-seq of AID-expressing cells from mice infected with WT or M2.Stop 73.Bla MHV68

Project description:Gammaherpesviruses (GHV) are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus (EBV) and murine gammaherpesvirus 68 (MHV68), this is accomplished through a viral gene-expression program that promotes cellular proliferation and differentiation, especially of germinal center (GC) B cells. Intrinsic host mechanisms to control virus-driven cellular expansion are incompletely defined. Using a small-animal model of GHV pathogenesis, we identify the B cell-specific latency gene M2, an MHV68 mediator of GC B cell differentiation, as a viral gene product that is sufficient to induce p53 in a manner that is dependent on Src kinase activity. To understand the function of M2 in germinal center B cells in vivo, we infected AID-cre tdTomato reporter mice with WT or M2.Stop 73.Bla MHV68. At 16 dpi, draining lymph nodes were harvested and treated with CCF4-AM. AID+ and AID+Bla+ lymphocytes were sorted from WT and M2.Stop MHV68 infected tissue and sent for ultra-low input RNA-seq analysis.

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RNA-seq on MHV68 infected GC B cells expressing distinct immunoglobulin light chains

Project description:We performed RNA-seq to examine the differences in GC B cells that were either infected with MHV68 or uninfected and between B cells that expressed IgL or IgK B cell receptor light chains.

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