Viral RNA-binding protein KSHV ORF57 and host transcriptome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA744781 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15069592_1.fastq.gz | Fastqsanger.gz | |||
| SRR15069592_2.fastq.gz | Fastqsanger.gz | |||
| SRR15069593_1.fastq.gz | Fastqsanger.gz | |||
| SRR15069593_2.fastq.gz | Fastqsanger.gz | |||
| SRR15069594_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Kaposi's sarcoma-associated herpesvirus (KSHV) encodes a viral RNA-binding protein ORF57 that plays an essential role in posttranscriptional regulation of viral gene expression. Ectopice expression of KSHV ORF57 in HEK293T cells was evaluated on its effect on host gene expression in the study, with the cells transfected with an empty vector serving as a control.
2023-02-13 | GSE179728 | GEO
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
Project description:Kaposi's sarcoma-associated virus (KSHV) ORF57 is a viral RNA-binding protein required for proper posttranscriptional processing of viral transcripts including RNA splicing. To identify the viral splicing events regulated by ORF57 we performed a genome-wide analysis of RNA splicing of viral RNAs in wild type (WT) versus ORF57 knock-out (57KO) primary effusion lymphoma cells line BCBL-1 after induction of KSHV lytic replication by 24h treatment with valproic acid (VA).
2022-06-16 | GSE194239 | GEO
Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is a human oncogenic virus associated with various malignancies, including Kaposi’s sarcoma, primary effusion lymphoma, and multicentric Castleman’s disease. The expression of viral products is essential for initiating and sustaining KSHV-induced tumors. KSHV ORF57, a viral RNA-binding protein, plays a crucial role in regulating viral gene expression at the posttranscriptional level by promoting viral RNA stability, splicing, and translation. In addition, ORF57 dysregulates host gene expression to promote viral replications.
2024-11-21 | GSE259446 | GEO
Project description:The Kaposi's sarcoma associated herpesvirus (KSHV) is an oncogenic virus that causes Kaposi's sarcoma, primary effusion lymphoma (PEL), and some forms of multicentric Castleman's disease. The KSHV ORF57 protein is a conserved posttranscriptional regulator of gene expression that is essential for virus replication. ORF57 is multifunctional, but most of its activities are directly linked to its ability to bind RNA. We globally identified virus and host RNAs bound by ORF57 during lytic reactivation in PEL cells using high-throughput sequencing of RNA isolated by crosslinking immunoprecipitation (HITS-CLIP). As expected, ORF57-bound RNA fragments mapped throughout the KSHV genome, including the known ORF57 ligand PAN RNA. In agreement with previously published ChIP results, we observed that ORF57 bound RNAs near the oriLyt regions of the genome. Examination of the host RNA fragments revealed that a subset of the ORF57-bound RNAs was derived from transcript 5´ ends. The position of these 5´-bound fragments correlated closely with the 5´-most exonintron junction of the pre-mRNA. We selected four candidates (BTG1, EGR1, ZFP36, and TNFSF9) and analyzed their pre-mRNA and mRNA levels during lytic phase. Analysis of both steady-state and newly made RNAs revealed that these candidate ORF57-bound pre-mRNAs persisted for longer periods of time throughout infection than control RNAs, consistent with a role for ORF57 in pre-mRNA metabolism. In addition, exogenous expression of ORF57 was sufficient to increase the pre-mRNA levels and, in one case, the mRNA levels of the putative ORF57 targets. These results demonstrate that ORF57 interacts with specific host pre-mRNAs during lytic reactivation and alters their processing, likely by stabilizing pre-mRNAs. These data suggest that ORF57 is involved in modulating host gene expression in addition to KSHV gene expression during lytic reactivation. HITS-CLIP was performed on TREx BCBL-Rta cells 20 hpi using antibodies against ORF57. Three biological replicates were performed.
2015-02-01 | E-GEOD-64413 | biostudies-arrayexpress
Project description:The Kaposi's sarcoma associated herpesvirus (KSHV) is an oncogenic virus that causes Kaposi's sarcoma, primary effusion lymphoma (PEL), and some forms of multicentric Castleman's disease. The KSHV ORF57 protein is a conserved posttranscriptional regulator of gene expression that is essential for virus replication. ORF57 is multifunctional, but most of its activities are directly linked to its ability to bind RNA. We globally identified virus and host RNAs bound by ORF57 during lytic reactivation in PEL cells using high-throughput sequencing of RNA isolated by crosslinking immunoprecipitation (HITS-CLIP). As expected, ORF57-bound RNA fragments mapped throughout the KSHV genome, including the known ORF57 ligand PAN RNA. In agreement with previously published ChIP results, we observed that ORF57 bound RNAs near the oriLyt regions of the genome. Examination of the host RNA fragments revealed that a subset of the ORF57-bound RNAs was derived from transcript 5´ ends. The position of these 5´-bound fragments correlated closely with the 5´-most exonintron junction of the pre-mRNA. We selected four candidates (BTG1, EGR1, ZFP36, and TNFSF9) and analyzed their pre-mRNA and mRNA levels during lytic phase. Analysis of both steady-state and newly made RNAs revealed that these candidate ORF57-bound pre-mRNAs persisted for longer periods of time throughout infection than control RNAs, consistent with a role for ORF57 in pre-mRNA metabolism. In addition, exogenous expression of ORF57 was sufficient to increase the pre-mRNA levels and, in one case, the mRNA levels of the putative ORF57 targets. These results demonstrate that ORF57 interacts with specific host pre-mRNAs during lytic reactivation and alters their processing, likely by stabilizing pre-mRNAs. These data suggest that ORF57 is involved in modulating host gene expression in addition to KSHV gene expression during lytic reactivation.
2015-02-01 | GSE64413 | GEO
Project description:Latency-associated nuclear antigen (LANA), a multifunctional protein expressed by the Kaposi sarcoma-associated herpesvirus (KSHV) in latently-infected cells, is required for stable maintenance of the viral episome. This is mediated by two interactions: LANA binds to specific sequences (LBS1 and 2) on viral DNA, and also engages host histones, tethering the viral genome to host chromosomes in mitosis. LANA has also been suggested to affect host gene expression, but both the mechanism(s) and role of this dysregulation in KSHV biology remain unclear. Here we have examined LANA interactions with host chromatin on a genome-wide scale using ChIP-seq, and show that LANA predominantly targets human genes near their transcriptional start sites (TSSs). These host LANA-binding sites are generally found within transcriptionally active promoters and display striking overrepresentation of a consensus DNA sequence virtually identical to the LBS1 motif in KSHV DNA. Comparison of the ChIP-seq profile with whole transcriptome (RNA-seq) data reveals that few of the genes that are differentially regulated in latent infection are occupied by LANA at their promoters. This suggests that direct LANA binding to promoters is not the prime determinant of altered host transcription in KSHV-infected cells. Most surprisingly, the association of LANA to both host and viral DNA is strongly disrupted during the lytic cycle of KSHV. This disruption can be prevented by the inhibition of viral DNA synthesis, suggesting the existence of novel and potent regulatory mechanisms linked to either viral DNA replication or late gene expression. Profiling of KSHV LANA positioning on the host genome and examination of gene expression from promoters bound by KSHV LANA.
2014-04-01 | E-GEOD-56144 | biostudies-arrayexpress
Project description:CLIP-seq analysis of KSHV ORF57-associated RNAs
| PRJNA744779 | ENA
Project description:Latency-associated nuclear antigen (LANA), a multifunctional protein expressed by the Kaposi sarcoma-associated herpesvirus (KSHV) in latently-infected cells, is required for stable maintenance of the viral episome. This is mediated by two interactions: LANA binds to specific sequences (LBS1 and 2) on viral DNA, and also engages host histones, tethering the viral genome to host chromosomes in mitosis. LANA has also been suggested to affect host gene expression, but both the mechanism(s) and role of this dysregulation in KSHV biology remain unclear. Here we have examined LANA interactions with host chromatin on a genome-wide scale using ChIP-seq, and show that LANA predominantly targets human genes near their transcriptional start sites (TSSs). These host LANA-binding sites are generally found within transcriptionally active promoters and display striking overrepresentation of a consensus DNA sequence virtually identical to the LBS1 motif in KSHV DNA. Comparison of the ChIP-seq profile with whole transcriptome (RNA-seq) data reveals that few of the genes that are differentially regulated in latent infection are occupied by LANA at their promoters. This suggests that direct LANA binding to promoters is not the prime determinant of altered host transcription in KSHV-infected cells. Most surprisingly, the association of LANA to both host and viral DNA is strongly disrupted during the lytic cycle of KSHV. This disruption can be prevented by the inhibition of viral DNA synthesis, suggesting the existence of novel and potent regulatory mechanisms linked to either viral DNA replication or late gene expression.
2014-04-01 | GSE56144 | GEO
Project description:Kaposi’s Sarcoma-associated herpesvirus (KSHV) transcripts are subject to degradation by at least two host-mediated nuclear RNA decay pathways, PABPN1 and PAPα/γ-mediated RNA decay (PPD) and an ARS2-dependent decay pathway. KSHV expresses the multifunctional protein ORF57, which increases viral transcripts stability by protecting them preferentially from ARS2-dependent decay. However, a subset of viral transcripts succumb to PPD even in the presence of ORF57, but the role of PPD during KSHV infection is not completely understood. We inactivated both decay pathways using siRNA and monitored their contribution to viral gene expression in the presence of ORF57 by RNA-Seq at 24 hours post induction (hpi). Inactivation of PPD, but not ARS2-mediated decay, results in aberrant accumulation of late transcripts, which are typically expressed at 48 hpi. PPD exerts its functions post-transcriptionally as the upregulation of late genes is independent of viral transactivation factors needed for their expression. Remarkably, at their proper time of expression, PPD inactivation has no effect on late transcripts. We further show that PPD evasion by late transcripts requires the host factor NRDE2. In conclusion, our studies show that KSHV uses PPD to fine-tune the temporal expression of its genes by preventing their premature accumulation.
2020-04-28 | GSE144747 | GEO