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

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

PROVIDER: PRJNA1201157 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31793721_1.fastq.gz	Fastqsanger.gz
	SRR31793721_2.fastq.gz	Fastqsanger.gz
	SRR31793722_1.fastq.gz	Fastqsanger.gz
	SRR31793722_2.fastq.gz	Fastqsanger.gz
	SRR31793723_1.fastq.gz	Fastqsanger.gz

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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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