Viral reprogramming of host transcription initiation [ATAC-seq]
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ABSTRACT:
PROVIDER: PRJNA1001910 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25512053_1.fastq.gz | Fastqsanger.gz | |||
| SRR25512053_2.fastq.gz | Fastqsanger.gz | |||
| SRR25512054_1.fastq.gz | Fastqsanger.gz | |||
| SRR25512054_2.fastq.gz | Fastqsanger.gz | |||
| SRR25512055_1.fastq.gz | Fastqsanger.gz |
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Project description:Viruses are master remodelers of the host cell environment in support of infection and virus production. For example, viruses typically regulate cell gene expression through modulating canonical cell promoter activity. Here, we show that Epstein Barr virus (EBV) replication causes “de novo” transcription initiation at 29,674 new transcription start sites throughout the cell genome. De novo transcription initiation is facilitated in part by the unique properties of the viral pre-initiation complex (vPIC) that binds a TATT[T/A]AA, TATA box-like sequence and activates transcription with minimal support by additional transcription factors. Other de novo promoters are driven by the viral transcription factors, Zta and Rta and are influenced by directional proximity to existing canonical cell promoters, a configuration that fosters transcription through existing promoters and transcriptional interference. These studies reveal a new way that viruses interact with the host transcriptome and shed light on primal features driving promoter function.
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Project description:Viruses are master remodelers of the host cell environment in support of infection and virus production. For example, viruses typically regulate cell gene expression through modulating canonical cell promoter activity. Here, we show that Epstein Barr virus (EBV) replication causes “de novo” transcription initiation at 29,674 new transcription start sites throughout the cell genome. De novo transcription initiation is facilitated in part by the unique properties of the viral pre-initiation complex (vPIC) that binds a simple TATT[T/A]AA, TATA box-like sequence and activates transcription with minimal support by additional transcription factors. Other de novo promoters are driven by the viral transcription factors, Zta and Rta and are influenced by directional proximity to existing canonical cell promoters, a configuration that fosters transcription through existing promoters and transcriptional interference. These studies reveal a new way that viruses interact with the host transcriptome and shed light on primal features driving promoter function.
2024-02-01 | GSE240011 | GEO
Project description:Viruses are master remodelers of the host cell environment in support of infection and virus production. For example, viruses typically regulate cell gene expression through modulating canonical cell promoter activity. Here, we show that Epstein Barr virus (EBV) replication causes “de novo” transcription initiation at 29,674 new transcription start sites throughout the cell genome. De novo transcription initiation is facilitated in part by the unique properties of the viral pre-initiation complex (vPIC) that binds a simple TATT[T/A]AA, TATA box-like sequence and activates transcription with minimal support by additional transcription factors. Other de novo promoters are driven by the viral transcription factors, Zta and Rta and are influenced by directional proximity to existing canonical cell promoters, a configuration that fosters transcription through existing promoters and transcriptional interference. These studies reveal a new way that viruses interact with the host transcriptome and shed light on primal features driving promoter function
2024-02-01 | GSE240008 | GEO
Project description:Viruses are master remodelers of the host cell environment in support of infection and virus production. For example, viruses typically regulate cell gene expression through modulating canonical cell promoter activity. Here, we show that Epstein Barr virus (EBV) replication causes “de novo” transcription initiation at 29,674 new transcription start sites throughout the cell genome. De novo transcription initiation is facilitated in part by the unique properties of the viral pre-initiation complex (vPIC) that binds a simple TATT[T/A]AA, TATA box-like sequence and activates transcription with minimal support by additional transcription factors. Other de novo promoters are driven by the viral transcription factors, Zta and Rta and are influenced by directional proximity to existing canonical cell promoters, a configuration that fosters transcription through existing promoters and transcriptional interference. These studies reveal a new way that viruses interact with the host transcriptome and shed light on primal features driving promoter function.
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Project description:Many viruses potently inhibit host protein synthesis while employing unconventional strategies to sustain their own translation, but how and why certain cellular mRNAs continue to be translated remains unclear. Here, we show that during shutoff by Vaccinia Virus (VacV) several host mRNAs increase in polysome occupancy but few, topped by JUN, result in increased protein abundance. Translation of viral mRNAs depended on the small ribosomal protein, Receptor for Activated C Kinase 1 (RACK1) and the eukaryotic Initiation Factor, eIF3. Cryo-electron microscopy (cryo-EM) further showed that eIF3 bound to virus-modified RACK1-containing 40S subunits that exhibit altered head rotation during infection. By contrast, RACK1 and eIF3 were dispensable for JUN translation. Moreover, structurally distinct 5’ untranslated regions (5’UTRs) in viral versus JUN mRNAs conferred differential eIF3 dependencies. Altogether, we reveal how distinct modes of non-canonical initiation support the production of both host and viral proteins that facilitate poxvirus replication despite infection-induced shutoff.
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Project description:Human papillomaviruses (HPVs) maintain their genomes as minichromosomes in the nuclei of infected keratinocytes. This study investigates the association of HPV31 genomes with host chromatin using both HiC and 4C-seq chromosome conformation capture techniques. We show that HPV31 genomes preferentially associate with transcriptionally active A compartments of host chromatin, regions of open chromatin defined by ATAC-seq, and super-enhancers defined by Brd4 and H3K27ac ChIP-seq. The viral genome association sites were also highly correlated with genomic loci previously identified as common HPV integration sites in cervical cancers. Recent studies have shown that transcriptionally active sites are prone to dsDNA breaks, and we find a strong correlation among dsBREAK datasets with transcriptionally active and open regions of host chromatin and the HPV31 genome association sites defined in our study. These findings suggest that HPV genomes associate with cellular transcriptional epicenters to maintain active viral gene expression during persistent infection, but also indicate that the susceptibility of these regions to dsDNA breaks could explain their propensity for viral DNA integration in HPV-associated cancers.
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