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

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

PROVIDER: PRJNA768614 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16186722_1.fastq.gz	Fastqsanger.gz
	SRR16186722_2.fastq.gz	Fastqsanger.gz
	SRR16186723_1.fastq.gz	Fastqsanger.gz
	SRR16186723_2.fastq.gz	Fastqsanger.gz
	SRR16186724_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 (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 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 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 (Omni-ATAC-seq II)

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