Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1140662 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30009763_1.fastq.gz | Fastqsanger.gz | |||
| SRR30009763_2.fastq.gz | Fastqsanger.gz | |||
| SRR30009764_1.fastq.gz | Fastqsanger.gz | |||
| SRR30009764_2.fastq.gz | Fastqsanger.gz | |||
| SRR30009765_1.fastq.gz | Fastqsanger.gz |
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Project description:Lytic replication is essential for persistent infection of Kaposi’s sarcoma-associated herpesvirus (KSHV) and the pathogenesis of related diseases, and many cellular pathways are hijacked by KSHV proteins to initiate and control the lytic replication of this virus. However, the machinery involved in KSHV lytic replication from the early to the late phases remains largely undetermined. We previously revealed that KSHV ORF45 plays important roles in late transcription and translation. In the present study, we reveal that the Forkhead box proteins FoxK1 and FoxK2 are ORF45-binding proteins and are essential for KSHV lytic gene expression and virion production and that depletion of FoxK1 or FoxK2 significantly suppresses the expression of many late viral genes. FoxK1 and FoxK2 directly bind to the promoters of several late viral genes, ORF45 augments the promoter binding and transcriptional activity of FoxK1 and FoxK2, and then FoxK1 or FoxK2 cooperates with ORF45 to promote late viral gene expression. Our findings suggest that ORF45 interacts with FoxK1 and FoxK2 and promotes their occupancy on a cluster of late viral promoters and their subsequent transcriptional activity; consequently FoxK1 and FoxK2 promote late gene expression to facilitate KSHV lytic replication.
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Project description:Assessment of the effect of Kaposi-sarcoma herpesvirus upon the transcriptome of lymphatic endothelial cells and its contribution to the transcriptome of Kaposi sarcoma.
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Project description:Cancer cells of primary effusion lymphoma (PEL) often contain both Kaposi sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV). We measured the interplay of human, KSHV, and EBV transcription in a cell culture model of PEL using single-cell RNA sequencing. The data detect widespread trace expression of lytic KSHV genes.
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Project description:Epstein Barr virus (EBV) replication contributes to multiple human diseases, including infectious mononucleosis, nasopharyngeal carcinoma, B-cell lymphomas, and oral hairy leukoplakia. We performed systematic quantitative analyses of temporal changes in host and EBV proteins during lytic replication to gain novel insights into virus-host interactions, using conditional Burkitt lymphoma models of type I and II EBV infection. We quantified profiles of >8000 cellular and 69 EBV proteins, including >500 plasma membrane proteins, providing temporal views of the lytic B-cell proteome and EBV virome. Our approach revealed EBV-induced remodelling of cell cycle, innate and adaptive immune pathways, including upregulation of the complement cascade and proteasomal degradation of the B-cell receptor complex, conserved between EBV types I and II. Cross-comparison with proteomic analyses of human cytomegalovirus infection and of a Kaposi sarcoma associated herpesvirus immunoevasin identified host factors targeted by multiple herpesviruses. Our results provide an important resource for studies of EBV replication.
2018-10-19 | PXD008752 | Pride
Project description:Epstein Barr virus (EBV) replication contributes to multiple human diseases, including infectious mononucleosis, nasopharyngeal carcinoma, B-cell lymphomas, and oral hairy leukoplakia. We performed systematic quantitative analyses of temporal changes in host and EBV proteins during lytic replication to gain novel insights into virus-host interactions, using conditional Burkitt lymphoma models of type I and II EBV infection. We quantified profiles of >8000 cellular and 69 EBV proteins, including >500 plasma membrane proteins, providing temporal views of the lytic B-cell proteome and EBV virome. Our approach revealed EBV-induced remodelling of cell cycle, innate and adaptive immune pathways, including upregulation of the complement cascade and proteasomal degradation of the B-cell receptor complex, conserved between EBV types I and II. Cross-comparison with proteomic analyses of human cytomegalovirus infection and of a Kaposi sarcoma associated herpesvirus immunoevasin identified host factors targeted by multiple herpesviruses. Our results provide an important resource for studies of EBV replication.
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Project description:Herpesviruses are a group of double-stranded DNA viruses known to develop versatile viral strategies to escape host immune surveillance for promoting their replication and propagation. This is illustrated by Kaposi’s sarcoma-associated herpesvirus (KSHV), an oncogenic gamma-herpesvirus that overcomes host immune suppression by multiple mechanisms. In this study, we reported that KSHV dysregulates 5-methylcytosine (m5C) modification and mRNA stability of host antiviral factors to benefit its lytic replication. KSHV lytic reactivation or de novo challenge led to downregulation of m5C RNA methyltransferases, NSUN2 and NSUN1 (NSUN2/1), while NSUN2/1 depletion promoted KSHV lytic replication. We further performed the RNA bisulfite sequencing (RNA-BS-seq) to identify KSHV-dependent m5C modification of host mRNAs. Overall, our results highlighted a new strategy for human gamma-herpesviruses to counteract host antiviral factors and promote their lytic replication by manipulating host m5C RNA methylation.
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Project description:Gene transcription is a highly regulated process, and deregulation of transcription factors activity underlie numerous pathologies including cancer. FOXK1 and FOXK2 (FOXK1/2) transcription factors have recently emerged as important regulators of cell metabolism, autophagy and cell differentiation. While FOXK1/2 possesses many overlapping functions in normal biology, their specific functions as well as deregulation of their transcriptional activity in cancer is less clear and often contradictory. FOXK1, but less FOXK2, is known to have oncogenic properties as higher expression levels of FOXK1 has been observed in several cancers and is correlated with tumor progression, invasion, and metastasis. However, the molecular mechanism by which FOXK1 exert its oncogenic properties in caner remains unknown. Here we show that elevated expression of FOXK1, but not FOXK2, in normal human fibroblasts promotes transcription of E2F target genes associated with increased proliferation and delayed senescence entry. Fibroblasts overexpressing FOXK1 are also more prone to cellular transformation with minimal oncogenic combinations, suggesting important oncogenic proprieties of FOXK1. Mechanistically, we found that FOXK1, but not FOXK2, is specifically modified by O-GlcNAcylation. FOXK1 O-GlcNAcylation is modulated during the cell cycle and its highest levels coincides with the G1/S phase transition. Moreover, FOXK1 O-GlcNAcylation is increased following cell transformation and loss of this modification leads to decreased FOXK1 ability to promote cellular transformation and tumor growth. Cells overexpressing FOXK1 O-GlcNAcylation-defective mutants have lower E2F1 expression, cell proliferation, and tumour growth. Our results define a distinct role of FOXK1 via O-GlcNAcylation in controlling the cell cycle through the orchestration of the E2F pathway.
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Project description:During lytic replication of Kaposi’s sarcoma-associated herpesvirus (KSHV), a nuclear viral long noncoding RNA known as PAN RNA becomes the most abundant polyadenylated transcript in the cell. Knockout or knockdown of KSHV PAN RNA results in loss of late lytic viral gene expression and, consequently, reduction of progeny virion release from the cell. We studied KSHV and RRV PAN RNA homologs using capture hybridization analysis of RNA targets (CHART) and observed their reproducible associations with host chromatin, but the loci differ between PAN RNA homologs.
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Project description:Primari effusion lymphoma are (PEL) patient-derived transformed B-cells harboring latent Kaposi's sarcoma-associated herpesvirus (KSHV). The treatment of PEL cells with valproic acid (VA) leads to reactivation of KSHV and viral lytic replication. The aim of this project is to evaluate the effect of KSHV lytic infection on expression of the host transcriptome.
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Project description:Kaposi's sarcoma-associated herpesvirus (KSHV) ORF57 is a viral RNA-binding protein essential for viral lytic gene expression. ORF57 binds to target RNA directly via interaction with cellular cofactors. To investigate the entire repertoire of ORF57-associated RNAs we performed UV cross-linking immunoprecipitatin (CLIP) experiment using an affinity-purified, highly specific anti-ORF57 antibody in KSHV-infected primariy effusion lymphoma BCBL-1 cells undegoing lytic virus replication.
2021-11-08 | GSE179726 | GEO