Influenza Virus Mounts a Two-Pronged Attack on Host RNA Polymerase II Transcription.
Influenza Virus Mounts a Two-Pronged Attack on Host RNA Polymerase II Transcription.
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DOI：
10.1016/j.celrep.2018.04.047
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发表时间：
2018-05-15
期刊：
影响因子：
8.8
通讯作者：
Fodor E
中科院分区：
文献类型：
--
作者：
Bauer DLV;Tellier M;Martínez-Alonso M;Nojima T;Proudfoot NJ;Murphy S;Fodor E
流感病毒与宿主RNA聚合酶II（Pol II）和mRNA加工机制密切相关。在这里，我们使用哺乳动物天然延伸转录测序（mNET-seq）来检查病毒感染期间Pol II的行为。我们表明，流感病毒执行一个双管齐下的主机转录攻击。首先，病毒感染导致转录起始位点下游的Pol II基因占据率降低。第二，病毒诱导的细胞应激导致PolII终止于poly（A）位点的灾难性失败，转录通常持续数十个酶。缺陷性Pol II终止的发生独立于病毒NS 1蛋白干扰宿主mRNA加工的能力。相反，这种终止缺陷是不同细胞应激的常见效应，并且是先前报道的基因下游转录物（DoG）产生的基础。我们的工作不仅对理解宿主-病毒相互作用，而且对理解哺乳动物转录的基本方面都有意义。流感病毒感染使宿主转录失调病毒感染从TSS下游的基因体中耗尽Pol II病毒诱导的应激导致Pol II终止的灾难性失败缺陷终止不需要病毒NS 1：宿主CPSF 30相互作用Bauer et al.研究流感病毒感染对宿主RNA聚合酶II（Pol II）全基因组转录的影响。他们发现，感染导致基因起始和末端的失调。他们的工作提供了深入了解病毒-宿主相互作用和哺乳动物转录的基本机制。
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. Influenza virus infection dysregulates host transcription Viral infection depletes Pol II from gene bodies downstream of the TSS Virus-induced stress leads to a catastrophic failure of Pol II termination Defective termination does not require viral NS1: host CPSF30 interaction Bauer et al. investigate the effects of influenza virus infection on host RNA polymerase II (Pol II) transcription genome-wide. They find that infection leads to dysregulation at both the starts and ends of genes. Their work provides insight into both virus-host interactions and fundamental mechanisms of mammalian transcription.
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3'RNA聚合酶II CTD上Ser2的前MRNA的末端形成和在人类细胞中相互耦合。
影响因子：
10.5
作者：
Davidson L;Muniz L;West S
通讯作者：
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DOI：
10.1126/science.aao6535
发表时间：
2017-11-24
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Casañal A;Kumar A;Hill CH;Easter AD;Emsley P;Degliesposti G;Gordiyenko Y;Santhanam B;Wolf J;Wiederhold K;Dornan GL;Skehel M;Robinson CV;Passmore LA
通讯作者：
Passmore LA
影响因子：
10.5
作者：
Eaton JD;Davidson L;Bauer DLV;Natsume T;Kanemaki MT;West S
通讯作者：
West S
影响因子：
7
作者：
Harrow J;Frankish A;Gonzalez JM;Tapanari E;Diekhans M;Kokocinski F;Aken BL;Barrell D;Zadissa A;Searle S;Barnes I;Bignell A;Boychenko V;Hunt T;Kay M;Mukherjee G;Rajan J;Despacio-Reyes G;Saunders G;Steward C;Harte R;Lin M;Howald C;Tanzer A;Derrien T;Chrast J;Walters N;Balasubramanian S;Pei B;Tress M;Rodriguez JM;Ezkurdia I;van Baren J;Brent M;Haussler D;Kellis M;Valencia A;Reymond A;Gerstein M;Guigó R;Hubbard TJ
通讯作者：
Hubbard TJ
影响因子：
7.7
作者：
Clerici M;Faini M;Aebersold R;Jinek M
通讯作者：
Jinek M