Leader-Containing Uncapped Viral Transcript Activates RIG-I in Antiviral Stress Granules.
Identifieur interne : 000B74 ( Main/Exploration ); précédent : 000B73; suivant : 000B75Leader-Containing Uncapped Viral Transcript Activates RIG-I in Antiviral Stress Granules.
Auteurs : Seong-Wook Oh [Japon] ; Koji Onomoto [Japon] ; Mai Wakimoto [Japon] ; Kazuhide Onoguchi [États-Unis] ; Fumiyoshi Ishidate [Japon] ; Takahiro Fujiwara [Japon] ; Mitsutoshi Yoneyama [Japon] ; Hiroki Kato [Japon] ; Takashi Fujita [Japon]Source :
- PLoS pathogens [ 1553-7374 ] ; 2016.
Descripteurs français
- KwdFr :
- ARN viral (), Animaux, DEAD-box RNA helicases (métabolisme), Facteur-3 de régulation d'interféron (métabolisme), Humains, Interféron bêta (), Interféron bêta (génétique), Interféron de type I (métabolisme), Protéine-58 à domaine DEAD, Souris, Stress physiologique, Transduction du signal (), Virus de la grippe A (génétique), Virus de la maladie de Newcastle (génétique).
- MESH :
- génétique : Interféron bêta, Virus de la grippe A, Virus de la maladie de Newcastle.
- métabolisme : DEAD-box RNA helicases, Facteur-3 de régulation d'interféron, Interféron de type I.
- ARN viral, Animaux, Humains, Interféron bêta, Protéine-58 à domaine DEAD, Souris, Stress physiologique, Transduction du signal.
English descriptors
- KwdEn :
- Animals, DEAD Box Protein 58, DEAD-box RNA Helicases (metabolism), Humans, Influenza A virus (genetics), Interferon Regulatory Factor-3 (metabolism), Interferon Type I (metabolism), Interferon-beta (drug effects), Interferon-beta (genetics), Mice, Newcastle disease virus (genetics), RNA, Viral (drug effects), Signal Transduction (drug effects), Stress, Physiological.
- MESH :
- chemical , drug effects : Interferon-beta, RNA, Viral.
- chemical , genetics : Interferon-beta.
- chemical , metabolism : DEAD-box RNA Helicases, Interferon Regulatory Factor-3, Interferon Type I.
- chemical : DEAD Box Protein 58.
- drug effects : Signal Transduction.
- genetics : Influenza A virus, Newcastle disease virus.
- Animals, Humans, Mice, Stress, Physiological.
Abstract
RIG-I triggers antiviral responses by recognizing viral RNA (vRNA) in the cytoplasm. However, the spatio-temporal dynamics of vRNA sensing and signal transduction remain elusive. We investigated the time course of events in cells infected with Newcastle disease virus (NDV), a non-segmented negative-strand RNA virus. RIG-I was recruited to viral replication complexes (vRC) and triggered minimal primary type I interferon (IFN) production. RIG-I subsequently localized to antiviral stress granules (avSG) induced after vRC formation. The inhibition of avSG attenuated secondary IFN production, suggesting avSG as a platform for efficient vRNA detection. avSG selectively captured positive-strand vRNA, and poly(A)+ RNA induced IFN production. Further investigations suggested that uncapped vRNA derived from read-through transcription was sensed by RIG-I in avSG. These results highlight how viral infections stimulate host stress responses, thereby selectively recruiting uncapped vRNA to avSG, in which RIG-I and other components cooperate in an efficient antiviral program.
DOI: 10.1371/journal.ppat.1005444
PubMed: 26862753
Affiliations:
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Laboratory of Molecular and Cellular Immunology, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Molecular Genetics, Institute for Virus Research; 2. Laboratory of Molecular and Cellular Immunology, Graduate School of Biostudies, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Onomoto, Koji" sort="Onomoto, Koji" uniqKey="Onomoto K" first="Koji" last="Onomoto">Koji Onomoto</name><affiliation wicri:level="1"><nlm:affiliation>Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba</wicri:regionArea><wicri:noRegion>Chiba</wicri:noRegion></affiliation></author><author><name sortKey="Wakimoto, Mai" sort="Wakimoto, Mai" uniqKey="Wakimoto M" first="Mai" last="Wakimoto">Mai Wakimoto</name><affiliation wicri:level="4"><nlm:affiliation>Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Onoguchi, Kazuhide" sort="Onoguchi, Kazuhide" uniqKey="Onoguchi K" first="Kazuhide" last="Onoguchi">Kazuhide Onoguchi</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, University of California, San Francisco, California, United States of America.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of California, San Francisco, California</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Ishidate, Fumiyoshi" sort="Ishidate, Fumiyoshi" uniqKey="Ishidate F" first="Fumiyoshi" last="Ishidate">Fumiyoshi Ishidate</name><affiliation wicri:level="3"><nlm:affiliation>Carl Zeiss MicroImaging Co., Ltd., Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Carl Zeiss MicroImaging Co., Ltd., Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Fujiwara, Takahiro" sort="Fujiwara, Takahiro" uniqKey="Fujiwara T" first="Takahiro" last="Fujiwara">Takahiro Fujiwara</name><affiliation wicri:level="4"><nlm:affiliation>Center for Meso-Bio Single-Molecule Imaging (CeMI), Institute for Integrated Cell-Material Sciences (iCeMS), Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Center for Meso-Bio Single-Molecule Imaging (CeMI), Institute for Integrated Cell-Material Sciences (iCeMS), Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Yoneyama, Mitsutoshi" sort="Yoneyama, Mitsutoshi" uniqKey="Yoneyama M" first="Mitsutoshi" last="Yoneyama">Mitsutoshi Yoneyama</name><affiliation wicri:level="1"><nlm:affiliation>Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba</wicri:regionArea><wicri:noRegion>Chiba</wicri:noRegion></affiliation></author><author><name sortKey="Kato, Hiroki" sort="Kato, Hiroki" uniqKey="Kato H" first="Hiroki" last="Kato">Hiroki Kato</name><affiliation wicri:level="4"><nlm:affiliation>Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Fujita, Takashi" sort="Fujita, Takashi" uniqKey="Fujita T" first="Takashi" last="Fujita">Takashi Fujita</name><affiliation wicri:level="4"><nlm:affiliation>Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author></analytic><series><title level="j">PLoS pathogens</title><idno type="eISSN">1553-7374</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>DEAD Box Protein 58</term><term>DEAD-box RNA Helicases (metabolism)</term><term>Humans</term><term>Influenza A virus (genetics)</term><term>Interferon Regulatory Factor-3 (metabolism)</term><term>Interferon Type I (metabolism)</term><term>Interferon-beta (drug effects)</term><term>Interferon-beta (genetics)</term><term>Mice</term><term>Newcastle disease virus (genetics)</term><term>RNA, Viral (drug effects)</term><term>Signal Transduction (drug effects)</term><term>Stress, Physiological</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN viral ()</term><term>Animaux</term><term>DEAD-box RNA helicases (métabolisme)</term><term>Facteur-3 de régulation d'interféron (métabolisme)</term><term>Humains</term><term>Interféron bêta ()</term><term>Interféron bêta (génétique)</term><term>Interféron de type I (métabolisme)</term><term>Protéine-58 à domaine DEAD</term><term>Souris</term><term>Stress physiologique</term><term>Transduction du signal ()</term><term>Virus de la grippe A (génétique)</term><term>Virus de la maladie de Newcastle (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Interferon-beta</term><term>RNA, Viral</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interferon-beta</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>DEAD-box RNA Helicases</term><term>Interferon Regulatory Factor-3</term><term>Interferon Type I</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>DEAD Box Protein 58</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A virus</term><term>Newcastle disease virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Interféron bêta</term><term>Virus de la grippe A</term><term>Virus de la maladie de Newcastle</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>DEAD-box RNA helicases</term><term>Facteur-3 de régulation d'interféron</term><term>Interféron de type I</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Mice</term><term>Stress, Physiological</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>ARN viral</term><term>Animaux</term><term>Humains</term><term>Interféron bêta</term><term>Protéine-58 à domaine DEAD</term><term>Souris</term><term>Stress physiologique</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">RIG-I triggers antiviral responses by recognizing viral RNA (vRNA) in the cytoplasm. However, the spatio-temporal dynamics of vRNA sensing and signal transduction remain elusive. We investigated the time course of events in cells infected with Newcastle disease virus (NDV), a non-segmented negative-strand RNA virus. RIG-I was recruited to viral replication complexes (vRC) and triggered minimal primary type I interferon (IFN) production. RIG-I subsequently localized to antiviral stress granules (avSG) induced after vRC formation. The inhibition of avSG attenuated secondary IFN production, suggesting avSG as a platform for efficient vRNA detection. avSG selectively captured positive-strand vRNA, and poly(A)+ RNA induced IFN production. Further investigations suggested that uncapped vRNA derived from read-through transcription was sensed by RIG-I in avSG. These results highlight how viral infections stimulate host stress responses, thereby selectively recruiting uncapped vRNA to avSG, in which RIG-I and other components cooperate in an efficient antiviral program. </div></front></TEI><affiliations><list><country><li>Japon</li><li>États-Unis</li></country><region><li>Californie</li><li>Région de Kantō</li><li>Région du Kansai</li></region><settlement><li>Kyoto</li><li>Tokyo</li></settlement><orgName><li>Université de Kyoto</li></orgName></list><tree><country name="Japon"><region name="Région du Kansai"><name sortKey="Oh, Seong Wook" sort="Oh, Seong Wook" uniqKey="Oh S" first="Seong-Wook" last="Oh">Seong-Wook Oh</name></region><name sortKey="Fujita, Takashi" sort="Fujita, Takashi" uniqKey="Fujita T" first="Takashi" last="Fujita">Takashi Fujita</name><name sortKey="Fujiwara, Takahiro" sort="Fujiwara, Takahiro" uniqKey="Fujiwara T" first="Takahiro" last="Fujiwara">Takahiro Fujiwara</name><name sortKey="Ishidate, Fumiyoshi" sort="Ishidate, Fumiyoshi" uniqKey="Ishidate F" first="Fumiyoshi" last="Ishidate">Fumiyoshi Ishidate</name><name sortKey="Kato, Hiroki" sort="Kato, Hiroki" uniqKey="Kato H" first="Hiroki" last="Kato">Hiroki Kato</name><name sortKey="Onomoto, Koji" sort="Onomoto, Koji" uniqKey="Onomoto K" first="Koji" last="Onomoto">Koji Onomoto</name><name sortKey="Wakimoto, Mai" sort="Wakimoto, Mai" uniqKey="Wakimoto M" first="Mai" last="Wakimoto">Mai Wakimoto</name><name sortKey="Yoneyama, Mitsutoshi" sort="Yoneyama, Mitsutoshi" uniqKey="Yoneyama M" first="Mitsutoshi" last="Yoneyama">Mitsutoshi Yoneyama</name></country><country name="États-Unis"><region name="Californie"><name sortKey="Onoguchi, Kazuhide" sort="Onoguchi, Kazuhide" uniqKey="Onoguchi K" first="Kazuhide" last="Onoguchi">Kazuhide Onoguchi</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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