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Human cytomegalovirusinduces neuronal geneexpression to promote virionmaturationin macroH2A1-dependent manner

ABSTRACT: Human cytomegalovirusinduces neuronal geneexpression to promote virionmaturationin macroH2A1-dependent manner

PROVIDER: PRJNA1135976 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29834500_1.fastq.gz	Fastqsanger.gz
	SRR29834500_2.fastq.gz	Fastqsanger.gz
	SRR29834501_1.fastq.gz	Fastqsanger.gz
	SRR29834501_2.fastq.gz	Fastqsanger.gz
	SRR29834502_1.fastq.gz	Fastqsanger.gz

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Human cytomegalovirusinduces neuronal geneexpression to promote virionmaturationin macroH2A1-dependent manner

Project description:Human cytomegalovirus (HCMV) uniquely remodels host cells, generating a cytoplasmic viral-induced assembly compartment (vIAC) and a kidney-bean-shaped nucleus. How these stark morphology changes take place in the context of host gene regulation is still emerging. Here, we discovered that HCMV titers, but not virus particle numbers, were significantly reduced in the absence of the histone variant macroH2A1, indicating that macroH2A1 is essential for producing infectious progeny. Because virion maturation and cellular remodeling are closely linked processes, we used confocal and electron microscopy to define structural changes in the host cell. We uncovered that HCMV-induced reorganization of the host nucleus, cytoskeleton, and endoplasmic reticulum does not occur in the absence of macroH2A1. Furthermore, we discovered using RNA-seq that while all viral genes were highly expressed in the absence of macroH2A1, many HCMV-induced host genes were not. Hundreds of these HCMV-induced macroH2A1-dependent host genes are associated with neuronal synapse formation and vesicle trafficking. Knock-down during infection of several HCMV-induced neuronal genes resulted in malformed vIACs and smaller plaques, establishing their importance to HCMV infection. Together, our findings demonstrate that HCMV manipulates host gene expression to hijack the dormant neuronal secretory pathway for proper virion maturation.

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Human cytomegalovirus induces neuronal gene expression to promote virion maturation in macroH2A1-dependent manner

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The histone variant macroH2A1 regulates key genes for myogenic cell fusion in a splice-isoform dependent manner [RNA-Seq]

Project description:The histone variant macroH2A1 regulates key genes for myogenic cell fusion in a splice-isoform dependent manner [RNA-Seq]

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The histone variant macroH2A1 regulates key genes for myogenic cell fusion in a splice-isoform dependent manner [ChIP-Seq]

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Project description:MacroH2A histone variants have functions in differentiation, somatic cell reprogramming and cancer. However, at the present it is not clear how macroH2As affect gene regulation to exert these functions. Here, we have addressed the question of whether the two splice isoforms of macroH2A1 differentially regulate genes in a physiological context. We have focused on myotube formation that is a key process in embryonic myogenesis and highly relevant for muscle regeneration after acute or chronic injury. We have parted from the initial observation that loss of total macroH2A1 led to a change in the morphology of myotubes differentiated ex vivo that was indicative of reduced fusion. Individual perturbation of the two isoforms in myotubes forming in vitro from myogenic C2C12 cells showed an opposing phenotype with macroH2A1.1 enhancing and macroH2A1.2 reducing fusion. Transcriptomic analysis allowed us to associate this phenotype with the differential regulation of a subset of fusion-related genes encoding components of the extracellular matrix and cell surface receptors for adhesion. In conclusion, we describe for the first time splice isoform-specific phenotypes for the histone variant macroH2A1 in a physiologic process and provide evidence for a novel, yet unknown underlying molecular mechanism of gene regulation independent of PARP1.

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