HSV-1 infection induces a delay of promoter-proximal pausing linked to a shift of H2A.Z-containing +1 nucleosomes (ATAC-seq)

We investigated transposase accessible chromatin using ATAC-seq in mock and HSV-1 strain 17 infection and infection with several HSV-1 mutants. Overall design: We used different HSV-1 mutants that lack expression of certain IE genes or VHS and examined 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. ATAC-seq data for mock, WT strain 17 (+/- PAA) and delta-ICP0, delta-ICP22, delta-ICP7 and delta-vhs can also be found under accession GSE185234.

本研究采用ATAC-seq技术，对模拟感染对照组（mock）、单纯疱疹病毒1型（HSV-1）17株感染及数株HSV-1突变株感染的细胞样本中的转座酶可及染色质（transposase accessible chromatin）进行了分析。实验设计概述：我们选用了若干缺失即刻早期基因（IE基因）或VHS基因表达的HSV-1突变株，旨在探究受影响基因转录终止位点下游的染色质开放状态。以感染复数（MOI）为10的条件感染各突变株的细胞，每组设置2次生物学重复（ΔICP22突变株感染组设置4次生物学重复）。空白对照组、野生型17株（添加或不添加PAA）、ΔICP0、ΔICP22、ΔICP7及Δvhs的ATAC-seq数据，亦可于登录号GSE185234下获取。