Refine
Has Fulltext
- yes (8)
Is part of the Bibliography
- yes (8)
Document Type
- Journal article (7)
- Preprint (1)
Language
- English (8) (remove)
Keywords
- transcription (2)
- Antisense (1)
- BBC3 (1)
- C-terminal domain (1)
- DNA transcription (1)
- HHV-6 (1)
- Herpes (1)
- Herpesvirus (1)
- ICP27 (1)
- ICP4 (1)
- IncRNA (1)
- NFKB (1)
- RNA polymerase II (1)
- Transcription (1)
- Virology (1)
- Virus (1)
- binding protein (1)
- biochemical assays (1)
- cellular stress responses (1)
- characterization and analytical techniques (1)
- chromatin (1)
- dogs (1)
- domain (1)
- expression (1)
- fusion and fission (1)
- gene expression (1)
- genetics (1)
- herpes simplex virus (1)
- herpes virus (1)
- histones (1)
- host shutoff (1)
- identification (1)
- immunology (1)
- infected-cell protein (1)
- latency (1)
- magnetic properties and materials (1)
- messenger RNA (1)
- miR-30 (1)
- miRNA processing (1)
- microbiology (1)
- mitochondria (1)
- molecular biology (1)
- murine cytomegalovirus (MCMV) (1)
- nanoparticles (1)
- parasitology (1)
- polyadenylation (1)
- promoter-proximal pausing (1)
- sequence (1)
- splicing (1)
- thermal stresses (1)
- transcriptional termination (1)
- translation (1)
- type 1 (1)
- type I interferon (1)
- virology (1)
- virus reactivation (1)
Institute
EU-Project number / Contract (GA) number
- 721016 (3)
- 101041177 (1)
- CoG 721016–HERPES (1)
- ERC-2016-CoG 721016-HERPES (1)
Herpes simplex virus 1 (HSV-1) infection and stress responses disrupt transcription termination by RNA Polymerase II (Pol II). In HSV-1 infection, but not upon salt or heat stress, this is accompanied by a dramatic increase in chromatin accessibility downstream of genes. Here, we show that the HSV-1 immediate-early protein ICP22 is both necessary and sufficient to induce downstream open chromatin regions (dOCRs) when transcription termination is disrupted by the viral ICP27 protein. This is accompanied by a marked ICP22-dependent loss of histones downstream of affected genes consistent with impaired histone repositioning in the wake of Pol II. Efficient knock-down of the ICP22-interacting histone chaperone FACT is not sufficient to induce dOCRs in ΔICP22 infection but increases dOCR induction in wild-type HSV-1 infection. Interestingly, this is accompanied by a marked increase in chromatin accessibility within gene bodies. We propose a model in which allosteric changes in Pol II composition downstream of genes and ICP22-mediated interference with FACT activity explain the differential impairment of histone repositioning downstream of genes in the wake of Pol II in HSV-1 infection.