@article{10.1371-journal.ppat.1006954,
    author = {Hennig, Thomas AND Michalski, Marco AND Rutkowski, Andrzej J. AND Djakovic, Lara AND Whisnant, Adam W. AND Friedl, Marie-Sophie AND Jha, Bhaskar Anand AND Baptista, Marisa A. P. AND L’Hernault, Anne AND Erhard, Florian AND Dölken, Lars AND Friedel, Caroline C.},
    journal = {PLOS Pathogens},
    publisher = {Public Library of Science},
    title = {HSV-1-induced disruption of transcription termination resembles a cellular stress response but selectively increases chromatin accessibility downstream of genes},
    year = {2018},
    month = {03},
    volume = {14},
    url = {https://doi.org/10.1371/journal.ppat.1006954},
    pages = {1-27},
    abstract = {Author summary Recently, we reported that productive herpes simplex virus 1 (HSV-1) infection leads to disruption of transcription termination (DoTT) of most but not all cellular genes. This results in extensive transcription beyond poly(A) sites and into downstream genes. Subsequently, cellular stress responses were found to trigger transcription downstream of genes (DoG) for >10% of protein-coding genes. Here, we directly compared the two phenomena in HSV-1 infection, salt and heat stress and observed significant overlaps between the affected genes. We speculate that HSV-1 either directly usurps a cellular stress response or disrupts the transcription termination machinery in other ways with similar consequences. In addition, we show that inhibition of calcium signaling does not specifically inhibit stress-induced DoG transcription but globally impairs RNA polymerase I, II and III transcription. Finally, HSV-1-induced DoTT, but not stress-induced DoG transcription, was accompanied by a strong increase in chromatin accessibility downstream of affected poly(A) sites. In its kinetics and extent, this essentially matched poly(A) read-through transcription but does not cause but rather requires DoTT. We hypothesize that this results from impaired histone repositioning when RNA Polymerase II enters downstream intergenic regions of genes affected by DoTT.},
    number = {3},
    doi = {10.1371/journal.ppat.1006954}
}