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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ChIPmentation)

ABSTRACT: The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ChIPmentation)

PROVIDER: PRJNA768407 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16188500_1.fastq.gz	Fastqsanger.gz
	SRR16188500_2.fastq.gz	Fastqsanger.gz
	SRR16188501_1.fastq.gz	Fastqsanger.gz
	SRR16188501_2.fastq.gz	Fastqsanger.gz
	SRR16188502_1.fastq.gz	Fastqsanger.gz

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ChIPmentation)

Project description:To look at the deposition of the histone marks in the downstream regions of DoTT genes, HFFF cells were either mock, WT HSV-1 (strain F and 17) or ΔICP22 virus infected. Throught the course of infection (for the marked samples), cells were treated with 350 ug/ml PAA. Samples were processed according to the original ChIPmentation protocol (Schmidl C et al. ChIPmentation: fast, robust, low-input ChIP-seq for histones and transcription factors. Nat Methods. 2015) with few changes as explained in the Materials and Methods section.

2023-06-20 | GSE185246 | GEO

The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (RNA-seq)

Project description:Primary human fetal foreskin fibroblasts (HFFF) were infected with the ICP22-null mutant of HSV-1 and HSV-1 Wt strain F at a multiplicity of infection (MOI) of 10 for 8 and 12 hpi. Cells were treated for 8 or 12 hours with the phosphonoacetic acid (PAA) (350ug/ml). Total cellular RNA was isolated using Trizol. T-HF cells were grown either in the presence or absence of DOX. Upon DOX exposure, cells expressed either HA-ICP22 or HA-ICP22 and V5-ICP27. T-HF HA-ICP22 cells were treated with 80 mM KCl (salt stress) for 2 hours before collecting the total RNA. Total cellular RNA was isolated using Trizol.

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ATAC-seq I)

Project description:We report that HSV-1 gives rise to transposase accessible chromatin in gene downstream areas, in regions that show transcription termination defects. We show that the viral protein ICP22 is responsible for this open chromatin.

2023-06-20 | GSE185234 | GEO

The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes

Project description:The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (Omni-ATAC-seq III)

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ATAC-seq II)

Project description:Primary human fetal foreskin fibroblasts (HFFF) were infected with wild-type simplex virus 1 (HSV-1) strain F and null-ICP22 mutant at a multiplicity of infection (MOI) of 10. ATAC-seq libraries were prepared starting with 50,000 cells per condition following the protocol described by Buenrostro et al., Nature Methods 2013

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (RNA-seq)

Project description:The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (RNA-seq)

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (RNA-seq II)

Project description:Part 1: Human telomerase reverse transcriptase (hTERT)-Immortalized cell line (T-HF) inducibly expressing ICP22 or ICP27 (doxycycline-induced) were analyzed for gene expression and read-through transcription by RNA-seq (total RNA). This experiment was performed in parallel to the corresponding OMNI-ATACseq libraries in replicate wells. ICP22 or ICP27 expression was induced for 24 h prior to other treatments or harvest, respectively. ICP22 expressing cells were additionally treated with KCl (200 mM) or control for 2 h prior to harvest. Part 2: Human telomerase reverse transcriptase (hTERT)-Immortalized cell line (T-HF) doxycycline-inducibly expressing an artificial miRNA against SSRP1 (two separate cell lines expressing different amiRNAs) were mock, HSV-1 strain F wild type or US1 deletion mutant infected to analyze gene expression and read-through transcription. This experiment was performed in parallel to the corresponding OMNI-ATACseq libraries in replicate wells. Expression of amiRNAs was induced for 72 h prior to infection. Cells were inoculated for 1 h and then incubated for another 8 h. The experiment was conducted with PAA (350 ug/ml) treatment, which was added after the inoculum was removed, and doxycycline where indicated.

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ATAC-seq I)

Project description:The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (ATAC-seq I)

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The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (RNA-seq II)

Project description:The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (RNA-seq II)

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