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

ABSTRACT: 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 salt stress for 2 hours before proceeding with Omni-ATAC-seq. OMNI-ATAC-seq was conducted for the KOS1.1 strain and compared to a full US1 deletion mutant.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185238 | GEO | 2023/06/20

REPOSITORIES: GEO

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

Project description:Human telomerase reverse transcriptase (hTERT)-Immortalized cell line (T-HF) inducibly expressing ICP22 or ICP27 (doxycycline-induced) were analysed for downstream open chromation region (dOCR) formation. 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) for 2 h prior to harvest. OMNI-ATACseq libraries were prepared with 50000 cells/sample as described by Corces, M., Trevino, A., Hamilton, E. et al. An improved ATAC-seq protocol reduces background and enables interrogation of frozen tissues. Nat Methods 14, 959–962 (2017). https://doi.org/10.1038/nmeth.4396

2023-06-20 | GSE208077 | 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.

2023-04-19 | GSE185239 | GEO

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

Project description:Human telomerase reverse transcriptase (hTERT)-Immortalized cell line (T-HF) with or without DOX-induced KD of SSPR1 and SPT6 were infected with wild-type simplex virus 1 (HSV-1) strain F or with ICP22-null mutant at a multiplicity of infection (MOI) of 10. Omni-ATAC-seq libraries were prepared starting with 50,000 cells per condition following the protocol described by Corces, M., Trevino, A., Hamilton, E. et al. An improved ATAC-seq protocol reduces background and enables interrogation of frozen tissues. Nat Methods 14, 959–962 (2017). https://doi.org/10.1038/nmeth.4396

2023-06-20 | GSE185236 | GEO

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.

2023-06-20 | GSE208078 | GEO

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

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

| PRJNA858109 | ENA

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

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

| PRJNA768360 | ENA

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

Project description: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 (Omni-ATAC-seq I)

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

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

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 | GSE185240 | GEO

ICP22 of Herpes Simplex Virus 1 decreases RNA Polymerase Processivity

Project description:These data files consist of Illumina next seq 500 sequencing data from precision nuclear run-on and global nuclear run-on experiments conducted with human epithelial Hep2 cells that have been infected with human herpes simplex virus-1 (F) strain mutants. The results of these studies suggest that ICP22 is necessary for reducing Pol II processivity on the viral genome which results in its maintenance on the viral genome over the course of infection. While human reads continued to decrease over the time course of infection in the repair virus, this did not occur in the ICP22 deletion virus where over time the number of human reads increased over the time course of infection rather than decreasing. The effects of ICP22 deletion were separable from inhibiting HSV-1 DNA replication to the extent that ICP22 deletion resulted in a decrease in Pol levels only at 6 hpi and not at 3 hpi as was observed in the mutant

2022-01-05 | GSE169574 | GEO

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