GSE185239
The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (RNA-seq)
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. Overall design: 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. 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.