Influenza virus infection causes global RNAPII termination defects

Viral infection perturbs host cells and can be used to uncover regulatory mechanisms controlling cellular responses and susceptibility to infections. Using cell biological, biochemical, and genetic tools, we reveal that influenza A virus (IAV) infection induces global transcriptional defects at the...

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Autores: Zhao, Nan, Sebastiano, Vittorio, Moshkina, Natasha, Mena, Nacho, Hultquist, Judd, Jimenez-Morales, David, Ma, Yixuan, Rialdi, Alex, Albrecht, Randy, Fenouil, Romain, Sánchez-Aparicio, M. T., Ayllón Barasoain, Juan, Ravisankar, Sweta, Haddad, Bahareh, Ho, Sook-Yiun, Low, Diana, Jin, Jian, Yurchenko, Vyacheslav, Prinjha, Rab K., Tarakhovsky, Alexander, Squatrito, Massimo, Pinto, Dalila, Kimaada, Allette, Byun, Minji, Smith, Melissa Laird, Sebra, Robert, Guccione, Ernesto, Tumpey, Terrence, Krogan, Nevan, Greenbaum, Benjamin, van Bakel, Harm, García Sastre, Adolfo, Marazzi, Ivan
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2018
País:España
Institución:Universidad de Burgos (UBU)
Repositorio:Repositorio Institucional de la Universidad de Burgos (RIUBU)
OAI Identifier:oai:riubu.ubu.es:10259/10919
Acceso en línea:https://hdl.handle.net/10259/10919
Access Level:acceso abierto
Palabra clave:Virus
Poli ADP ribosa polimerasa
NAD-ADP-ribosyltransferase
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spelling Influenza virus infection causes global RNAPII termination defectsZhao, NanSebastiano, VittorioMoshkina, NatashaMena, NachoHultquist, JuddJimenez-Morales, DavidMa, YixuanRialdi, AlexAlbrecht, RandyFenouil, RomainSánchez-Aparicio, M. T.Ayllón Barasoain, JuanRavisankar, SwetaHaddad, BaharehHo, Sook-YiunLow, DianaJin, JianYurchenko, VyacheslavPrinjha, Rab K.Tarakhovsky, AlexanderSquatrito, MassimoPinto, DalilaKimaada, AlletteByun, MinjiSmith, Melissa LairdSebra, RobertGuccione, ErnestoTumpey, TerrenceKrogan, NevanGreenbaum, Benjaminvan Bakel, HarmGarcía Sastre, AdolfoMarazzi, IvanVirusPoli ADP ribosa polimerasaNAD-ADP-ribosyltransferaseViral infection perturbs host cells and can be used to uncover regulatory mechanisms controlling cellular responses and susceptibility to infections. Using cell biological, biochemical, and genetic tools, we reveal that influenza A virus (IAV) infection induces global transcriptional defects at the 3′ ends of active host genes and RNA polymerase II (RNAPII) run-through into extragenic regions. Deregulated RNAPII leads to expression of aberrant RNAs (3′ extensions and host-gene fusions) that ultimately cause global transcriptional downregulation of physiological transcripts, an effect influencing antiviral response and virulence. This phenomenon occurs with multiple strains of IAV, is dependent on influenza NS1 protein, and can be modulated by SUMOylation of an intrinsically disordered region (IDR) of NS1 expressed by the 1918 pandemic IAV strain. Our data identify a strategy used by IAV to suppress host gene expression and indicate that polymorphisms in IDRs of viral proteins can affect the outcome of an infection.We thank all members of the laboratories of I.M. and A.G.-S., and J. Bloom and A. Kornblihtt for valuable discussions and suggestions on the manuscript. We thank the Medicinal Chemistry Core, Integrated Screening Core, Microscopy CoRE,, and Global Health and Emerging Pathogens Institute (GHEPI) at the Icahn School of Medicine at Mount Sinai. H.v.B., I.M., and A.G.-S. are partially supported by HHSN272201400008C–Center for Research on Influenza Pathogenesis (CRIP), a NIAID-funded Center of Excellence for Influenza Research and Surveillance (CEIRS). I.M. is supported in part by the Department of Defense W911NF-14-1-0353. I.M. and H.v.B. are supported by NIH grant 1R01AN3663134. The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention/the Agency for Toxic Substances and Disease Registry. This work was supported in part through the computational resources and staff expertise provided by Scientific Computing at the Icahn School of Medicine at Mount Sinai.Nature Research202520252018info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionapplication/pdfhttps://hdl.handle.net/10259/10919reponame:Repositorio Institucional de la Universidad de Burgos (RIUBU)instname:Universidad de Burgos (UBU)InglésNature Structural and Molecular Biology. 2018, V. 25, n. 9, p. 885-893https://doi.org/10.1038/s41594-018-0124-7info:eu-repo/semantics/openAccessoai:riubu.ubu.es:10259/109192026-05-28T07:56:11Z
dc.title.none.fl_str_mv Influenza virus infection causes global RNAPII termination defects
title Influenza virus infection causes global RNAPII termination defects
spellingShingle Influenza virus infection causes global RNAPII termination defects
Zhao, Nan
Virus
Poli ADP ribosa polimerasa
NAD-ADP-ribosyltransferase
title_short Influenza virus infection causes global RNAPII termination defects
title_full Influenza virus infection causes global RNAPII termination defects
title_fullStr Influenza virus infection causes global RNAPII termination defects
title_full_unstemmed Influenza virus infection causes global RNAPII termination defects
title_sort Influenza virus infection causes global RNAPII termination defects
dc.creator.none.fl_str_mv Zhao, Nan
Sebastiano, Vittorio
Moshkina, Natasha
Mena, Nacho
Hultquist, Judd
Jimenez-Morales, David
Ma, Yixuan
Rialdi, Alex
Albrecht, Randy
Fenouil, Romain
Sánchez-Aparicio, M. T.
Ayllón Barasoain, Juan
Ravisankar, Sweta
Haddad, Bahareh
Ho, Sook-Yiun
Low, Diana
Jin, Jian
Yurchenko, Vyacheslav
Prinjha, Rab K.
Tarakhovsky, Alexander
Squatrito, Massimo
Pinto, Dalila
Kimaada, Allette
Byun, Minji
Smith, Melissa Laird
Sebra, Robert
Guccione, Ernesto
Tumpey, Terrence
Krogan, Nevan
Greenbaum, Benjamin
van Bakel, Harm
García Sastre, Adolfo
Marazzi, Ivan
author Zhao, Nan
author_facet Zhao, Nan
Sebastiano, Vittorio
Moshkina, Natasha
Mena, Nacho
Hultquist, Judd
Jimenez-Morales, David
Ma, Yixuan
Rialdi, Alex
Albrecht, Randy
Fenouil, Romain
Sánchez-Aparicio, M. T.
Ayllón Barasoain, Juan
Ravisankar, Sweta
Haddad, Bahareh
Ho, Sook-Yiun
Low, Diana
Jin, Jian
Yurchenko, Vyacheslav
Prinjha, Rab K.
Tarakhovsky, Alexander
Squatrito, Massimo
Pinto, Dalila
Kimaada, Allette
Byun, Minji
Smith, Melissa Laird
Sebra, Robert
Guccione, Ernesto
Tumpey, Terrence
Krogan, Nevan
Greenbaum, Benjamin
van Bakel, Harm
García Sastre, Adolfo
Marazzi, Ivan
author_role author
author2 Sebastiano, Vittorio
Moshkina, Natasha
Mena, Nacho
Hultquist, Judd
Jimenez-Morales, David
Ma, Yixuan
Rialdi, Alex
Albrecht, Randy
Fenouil, Romain
Sánchez-Aparicio, M. T.
Ayllón Barasoain, Juan
Ravisankar, Sweta
Haddad, Bahareh
Ho, Sook-Yiun
Low, Diana
Jin, Jian
Yurchenko, Vyacheslav
Prinjha, Rab K.
Tarakhovsky, Alexander
Squatrito, Massimo
Pinto, Dalila
Kimaada, Allette
Byun, Minji
Smith, Melissa Laird
Sebra, Robert
Guccione, Ernesto
Tumpey, Terrence
Krogan, Nevan
Greenbaum, Benjamin
van Bakel, Harm
García Sastre, Adolfo
Marazzi, Ivan
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Virus
Poli ADP ribosa polimerasa
NAD-ADP-ribosyltransferase
topic Virus
Poli ADP ribosa polimerasa
NAD-ADP-ribosyltransferase
description Viral infection perturbs host cells and can be used to uncover regulatory mechanisms controlling cellular responses and susceptibility to infections. Using cell biological, biochemical, and genetic tools, we reveal that influenza A virus (IAV) infection induces global transcriptional defects at the 3′ ends of active host genes and RNA polymerase II (RNAPII) run-through into extragenic regions. Deregulated RNAPII leads to expression of aberrant RNAs (3′ extensions and host-gene fusions) that ultimately cause global transcriptional downregulation of physiological transcripts, an effect influencing antiviral response and virulence. This phenomenon occurs with multiple strains of IAV, is dependent on influenza NS1 protein, and can be modulated by SUMOylation of an intrinsically disordered region (IDR) of NS1 expressed by the 1918 pandemic IAV strain. Our data identify a strategy used by IAV to suppress host gene expression and indicate that polymorphisms in IDRs of viral proteins can affect the outcome of an infection.
publishDate 2018
dc.date.none.fl_str_mv 2018
2025
2025
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/10259/10919
url https://hdl.handle.net/10259/10919
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Nature Structural and Molecular Biology. 2018, V. 25, n. 9, p. 885-893
https://doi.org/10.1038/s41594-018-0124-7
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Nature Research
publisher.none.fl_str_mv Nature Research
dc.source.none.fl_str_mv reponame:Repositorio Institucional de la Universidad de Burgos (RIUBU)
instname:Universidad de Burgos (UBU)
instname_str Universidad de Burgos (UBU)
reponame_str Repositorio Institucional de la Universidad de Burgos (RIUBU)
collection Repositorio Institucional de la Universidad de Burgos (RIUBU)
repository.name.fl_str_mv
repository.mail.fl_str_mv
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