期刊
JOURNAL OF GENERAL VIROLOGY
卷 89, 期 -, 页码 68-77出版社
MICROBIOLOGY SOC
DOI: 10.1099/vir.0.83272-0
关键词
-
资金
- MRC [MC_U130169964, G9800943] Funding Source: UKRI
- Medical Research Council [G9800943, MC_U130169964] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
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 histories at virus promoters. The fold change in association of pan-acetylated histone H3 following Ad.TRE.ICPO-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 ICPO expression is not uniformly targeted across the HSV-1 genome during ICPO-mediated derepression.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据