Histone modifications associated with herpes simplex virus type 1 genomes during quiescence and following ICP0-mediated de-repression.
Histone modifications associated with herpes simplex virus type 1 genomes during quiescence and following ICP0-mediated de-repression.
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DOI：
10.1099/vir.0.83272-0
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发表时间：
2008-01
期刊：
影响因子：
--
通讯作者：
Efstathiou S
中科院分区：
文献类型：
--
作者：
Coleman HM;Connor V;Cheng ZSC;Grey F;Preston CM;Efstathiou S
在目前的研究中，研究表明，在静止感染的MRC5细胞中，受抑制的病毒基因组采用一种受抑制的组蛋白相关结构，其特征是在多种单纯疱疹病毒1型（HSV-1）启动子上富集去乙酰化组蛋白。此外，研究表明，通过HSV-2重复感染或使用重组腺病毒载体传递ICP0介导的基因组去抑制可导致HSV DNA上乙酰化组蛋白的富集。这些数据表明，icp0介导的基因组去抑制与病毒启动子乙酰化组蛋白的富集密切相关。Ad.TRE后泛乙酰化组蛋白H3相关性的折叠变化。icp0介导的去抑制一致地揭示了启动子特异性变异，在潜伏期相关的转录启动子和增强子区域观察到最高的倍数变化（bbb50倍）。使用组蛋白H3 C端特异性抗体作为核小体占用率的替代测量的染色质免疫沉淀分析显示，在各种HSV启动子上，组蛋白H3的总负载几乎没有变化。这一观察结果表明，在ICP0介导的去抑制过程中，组蛋白H3乙酰化对ICP0表达的反应并不是整个HSV-1基因组的统一目标。
In the current study, it was shown that repressed virus genomes in quiescently infected MRC5 cells adopt a repressed histone-associated structure marked by the enrichment of deacetylated histones at a wide variety of herpes simplex virus type 1 (HSV-1) promoters. In addition, it was shown that genome de-repression, mediated by HSV-2 superinfection or delivery of ICP0 using a recombinant adenovirus vector, resulted in the enrichment of acetylated histones on HSV DNA. These data indicate that ICP0-mediated genome de-repression is intimately linked to enrichment of acetylated histones at virus promoters. The fold change in association of pan-acetylated histone H3 following Ad.TRE.ICP0-mediated de-repression consistently revealed promoter-specific variation, with the highest fold changes (>50-fold) being observed at the latency-associated transcript promoter and enhancer regions. Chromatin immunoprecipitation analyses using an antibody specific to the C terminus of histone H3 as a surrogate measure of nucleosome occupancy revealed little variability in the total loading of histone H3 at the various HSV promoters. This observation suggests that acetylation of histone H3 in response to ICP0 expression is not uniformly targeted across the HSV-1 genome during ICP0-mediated de-repression.
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