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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185234 | 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 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

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 (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

2023-06-20 | GSE185235 | 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 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 (Omni-ATAC-seq I)

Project description: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.

2023-06-20 | GSE185238 | GEO

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.

Project description:Herpes simplex virus 1 (HSV-1) infection and stress responses disrupt transcription termination by RNA Polymerase II (Pol II). In HSV-1 infection, but not upon salt or heat stress, this is accompanied by a dramatic increase in chromatin accessibility downstream of genes. Here, we show that the HSV-1 immediate-early protein ICP22 is both necessary and sufficient to induce downstream open chromatin regions (dOCRs) when transcription termination is disrupted by the viral ICP27 protein. This is accompanied by a marked ICP22-dependent loss of histones downstream of affected genes consistent with impaired histone repositioning in the wake of Pol II. Efficient knock-down of the ICP22-interacting histone chaperone FACT is not sufficient to induce dOCRs in ΔICP22 infection but increases dOCR induction in wild-type HSV-1 infection. Interestingly, this is accompanied by a marked increase in chromatin accessibility within gene bodies. We propose a model in which allosteric changes in Pol II composition downstream of genes and ICP22-mediated interference with FACT activity explain the differential impairment of histone repositioning downstream of genes in the wake of Pol II in HSV-1 infection.

| S-EPMC10390501 | biostudies-literature

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

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

| PRJNA768405 | ENA