@article{162811,
  keywords = {Animals, Promoter Regions, Genetic, Mice, Viral Proteins, Virus Replication, Herpesviridae Infections, Genome, Viral, NIH 3T3 Cells, Herpesvirus 8, Human, RNA Polymerase II, RNA Stability, Endonucleases, Rhadinovirus, Transcription Factor TFIIB},
  author = {Ella Hartenian and Sarah Gilbertson and Joel Federspiel and Ileana Cristea and Britt Glaunsinger},
  title = {RNA decay during gammaherpesvirus infection reduces RNA polymerase II occupancy of host promoters but spares viral promoters},
  abstract = {<p>In mammalian cells, widespread acceleration of cytoplasmic mRNA degradation is linked to impaired RNA polymerase II (Pol II) transcription. This mRNA decay-induced transcriptional repression occurs during infection with gammaherpesviruses including Kaposi{\textquoteright}s sarcoma-associated herpesvirus (KSHV) and murine gammaherpesvirus 68 (MHV68), which encode an mRNA endonuclease that initiates widespread RNA decay. Here, we show that MHV68-induced mRNA decay leads to a genome-wide reduction of Pol II occupancy at mammalian promoters. This reduced Pol II occupancy is accompanied by down-regulation of multiple Pol II subunits and TFIIB in the nucleus of infected cells, as revealed by mass spectrometry-based global measurements of protein abundance. Viral genes, despite the fact that they require Pol II for transcription, escape transcriptional repression. Protection is not governed by viral promoter sequences; instead, location on the viral genome is both necessary and sufficient to escape the transcriptional repression effects of mRNA decay. We propose a model in which the ability to escape from transcriptional repression is linked to the localization of viral DNA within replication compartments, providing a means for these viruses to counteract decay-induced transcript loss.</p>
},
  year = {2020},
  journal = {PLoS Pathog},
  volume = {16},
  pages = {e1008269},
  month = {02/2020},
  issn = {1553-7374},
  doi = {10.1371/journal.ppat.1008269},
  language = {eng},
}