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

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. We used different HSV-1 mutants that lack expression of certain IE genes or VHS and examine the opening of chromatin downstream of transcription termination sites of affected genes. Two biological replicates (four replicates for delta-ICP22) of cells infected with different HSV-1 mutants at MOI 10 were prepared.