期刊
CELL REPORTS
卷 23, 期 7, 页码 2119-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.04.047
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类别
资金
- Medical Research Council (MRC) [MR/K000241/1]
- EPA Cephalosporin Junior Research Fellowship
- Marie Curie Intra European Fellowship within the 7th European Community Framework Programme [PIEF-GA-2012-32 8746]
- European Research Council [339270]
- Wellcome Trust [090532/Z/09/Z, 107928/Z/15/Z, WT106134A]
- BBSRC [BB/R016836/1] Funding Source: UKRI
- MRC [G0400653, MR/K000241/1] Funding Source: UKRI
Influenza virus intimately associates with host RNA polymerase II (Pol II) and mRNA processing machinery. Here, we use mammalian native elongating transcript sequencing (mNET-seq) to examine Pol II behavior during viral infection. We show that influenza virus executes a two-pronged attack on host transcription. First, viral infection causes decreased Pol II gene occupancy downstream of transcription start sites. Second, virus-induced cellular stress leads to a catastrophic failure of Pol II termination at poly(A) sites, with transcription often continuing for tens of kilobases. Defective Pol II termination occurs independently of the ability of the viral NS1 protein to interfere with host mRNA processing. Instead, this termination defect is a common effect of diverse cellular stresses and underlies the production of previously reported downstream-of-gene transcripts (DoGs). Our work has implications for understanding not only host-virus interactions but also fundamental aspects of mammalian transcription.
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