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ABSTRACT: ICP4 ChIP-Seq of WT (KOS) HSV-1 Productive Infection in MRC5 cells

PROVIDER: PRJNA553563 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9661301.fastq.gz	Fastqsanger.gz
	SRR9661302.fastq.gz	Fastqsanger.gz
	SRR9661303.fastq.gz	Fastqsanger.gz
	SRR9661304.fastq.gz	Fastqsanger.gz
	SRR9661305.fastq.gz	Fastqsanger.gz

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Project description:Histone ChIP-Seq of WT (KOS) and ICP4 null (n12) HSV-1 Productive Infection in MRC5 cells

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Project description:GTF ChIP-Seq of WT (KOS) and ICP4 null (n12) HSV-1 Productive Infection in MRC5 cells

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Project description:ATAC-Seq of WT (KOS) and ICP4 null (n12) HSV-1 Productive Infection in MRC5 cells

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Genome-wide analysis of RNA polymerase II occupancy during HSV-1 infection in the presence and absence of ICP4.

Project description:The goal of this study was to identify how the occupancy of RNA polymerase II (Pol II) on the host genome changes during HSV-1 infection and is impacted by the viral immediate early protein ICP4. Pol II ChIP-seq experiments after infection with the wild-type (WT) virus and mutant ICP4 (n12) virus, compared to mock infection, revealed global increases and decreases in Pol II occupancy on the host genome that depended upon ICP4.

2021-07-07 | GSE171600 | GEO

Parallel G-quadruplexes recruit the HSV-1 transcription factor ICP4 to promote viral transcription in herpes virus-infected human cells

Project description:G-quadruplexes (G4s) are four-stranded nucleic acid structures abundant at gene promoters. They can adopt several distinctive conformations. G4s have been shown to form in the herpes simplex virus-1 (HSV-1) genome during its viral cycle. Here by cross-linking/pull-down assay we identified ICP4, the major HSV-1 transcription factor, as the protein that most efficiently interacts with viral G4s during infection. ICP4 specific and direct binding and unfolding of parallel G4s, including those present in HSV-1 immediate early gene promoters, induced transcription in vitro and in infected cells. This mechanism was also exploited by ICP4 to promote its own transcription. Proximity ligation assay allowed visualization of G4-protein interaction at the single selected G4 in cells. G4 ligands inhibited ICP4 binding to G4s. Our results indicate the existence of a well-defined G4-viral protein network that regulates the productive HSV-1 cycle. They also point to G4s as elements that recruit transcription factors to activate transcription in cells.

2021-09-10 | PXD024743 | Pride

RNAseq comparison of HSV-1 KOS vs n199 infected cells

Project description:The abundance of HSV mRNAs was determines over 16h of infection in wt (KOS) and n199 (ICP22 mutant) infected cells. ICP22 is an immediate early gene of HSV that affects gene expression

2018-01-20 | GSE109420 | GEO

Project description:ChIP-Seq of HSV-1 Productive Infection

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Project description:ChIP-Seq of HSV-1 (tsKos) Productive Infection

| PRJNA508791 | ENA

Project description:ChIP-Seq of HSV-1 Productive Infection +ACV

| PRJNA508766 | ENA

Transcriptomic analysis of early HSV-1 transcription in the absence of the immediate early protein, ICP4 [PROSeq]

Project description:Herpes simplex virus 1 (HSV-1) transcription is tightly regulated in a temporal cascade, utilizing cellular RNA polymerase (Pol). We previously observed that infection with HSV-1 mutants lacking immediate early (IE) genes a0, a4 and a22 exhibited unusually high levels of aberrant transcription across the viral genome at just 1.5 hpi. The strongest effect occurred in the absence of a4, which is both an essential transcriptional activator and repressor. The goal of the current study was to define the mechanism of ICP4-mediated early transcriptional repression on the viral genome. Using the transcriptomic tools PRO-Cap, PRO-Seq, GRO-Seq and Nanopore direct RNA sequencing we found that initiation was elevated at viral promoters of all temporal classes in the absence of ICP4. Despite higher levels of initiation, transcription of non-IE genes was stalled within gene bodies and did not lead to production of mature mRNA. We therefore posit that HSV-1 retains additional ICP4-independent mechanisms to limit expression of viral genes that initiate prematurely. The data also indicated rapid release from promoter proximal pausing and progression along HSV IE genes and revealed termination as an important rate -limiting regulatory step. These findings highlight multiple mechanisms that HSV-1 employs to regulate early transcription and identify ICP4’s repressive role is to restrict initiation on non IE genes, thereby ensuring correct progression of the temporal cascade.

2023-09-05 | GSE235227 | GEO

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