Severe Acute Respiratory Syndrome Coronavirus nsp1 Facilitates Efficient Propagation in Cells through a Specific Translational Shutoff of Host mRNA
Identifieur interne : 000036 ( PascalFrancis/Checkpoint ); précédent : 000035; suivant : 000037Severe Acute Respiratory Syndrome Coronavirus nsp1 Facilitates Efficient Propagation in Cells through a Specific Translational Shutoff of Host mRNA
Auteurs : Tomohisa Tanaka [Japon] ; Wataru Kamitani [Japon] ; Marta L. Dediego [Espagne] ; Luis Enjuanes [Espagne] ; Yoshiharu Matsuura [Japon]Source :
- Journal of virology [ 0022-538X ] ; 2012.
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- Pascal (Inist)
English descriptors
Abstract
Severe acute respiratory syndrome (SARS) coronavirus (SCoV) is an enveloped virus containing a single-stranded, positive-sense RNA genome. Nine mRNAs carrying a set of common 5' and 3' untranslated regions (UTR) are synthesized from the incoming viral genomic RNA in cells infected with SCoV. A nonstructural SCoV nsp1 protein causes a severe translational shutoff by binding to the 40S ribosomal subunits. The nsp1-40S ribosome complex further induces an endonucleolytic cleavage near the 5'UTR of host mRNA. However, the mechanism by which SCoV viral proteins are efficiently produced in infected cells in which host protein synthesis is impaired by nsp is unknown. In this study, we investigated the role of the viral UTRs in evasion of the nsp1-mediated shutoff. Luciferase activities were significantly suppressed in cells expressing nsp1 together with the mRNA carrying a luciferase gene, while nsp1 failed to suppress luciferase activities of the mRNA flanked by the 5'UTR of SCoV. An RNA-protein binding assay and RNA decay assay revealed that nsp1 bound to stem-loop 1 (SL1) in the 5'UTR of SCoV RNA and that the specific interaction with nsp1 stabilized the mRNA carrying SL1. Furthermore, experiments using an SCoV replicon system showed that the specific interaction enhanced the SCoV replication. The specific interaction of nsp1 with SL1 is an important strategy to facilitate efficient viral gene expression in infected cells, in which nsp1 suppresses host gene expression. Our data indicate a novel mechanism of viral gene expression control by nsp 1 and give new insight into understanding the pathogenesis of SARS.
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Dediego</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Department of Molecular and Cell Biology, Centro Nacional de Biotecnologia (CNB-CSIC), Campus Universidad Autonoma</s1><s2>Madrid</s2><s3>ESP</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Espagne</country><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author><author><name sortKey="Enjuanes, Luis" sort="Enjuanes, Luis" uniqKey="Enjuanes L" first="Luis" last="Enjuanes">Luis Enjuanes</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Department of Molecular and Cell Biology, Centro Nacional de Biotecnologia (CNB-CSIC), Campus Universidad Autonoma</s1><s2>Madrid</s2><s3>ESP</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Espagne</country><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author><author><name sortKey="Matsuura, Yoshiharu" sort="Matsuura, Yoshiharu" uniqKey="Matsuura Y" first="Yoshiharu" last="Matsuura">Yoshiharu Matsuura</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University</s1><s2>Osaka</s2><s3>JPN</s3><sZ>5 aut.</sZ></inist:fA14><country>Japon</country><wicri:noRegion>Osaka</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">12-0390363</idno><date when="2012">2012</date><idno type="stanalyst">PASCAL 12-0390363 INIST</idno><idno type="RBID">Pascal:12-0390363</idno><idno type="wicri:Area/PascalFrancis/Corpus">000046</idno><idno type="wicri:Area/PascalFrancis/Curation">000942</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000036</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000036</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Severe Acute Respiratory Syndrome Coronavirus nsp1 Facilitates Efficient Propagation in Cells through a Specific Translational Shutoff of Host mRNA</title><author><name sortKey="Tanaka, Tomohisa" sort="Tanaka, Tomohisa" uniqKey="Tanaka T" first="Tomohisa" last="Tanaka">Tomohisa Tanaka</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Global COE Program, Research Institute for Microbial Diseases, Osaka University</s1><s2>Osaka</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Japon</country><wicri:noRegion>Osaka</wicri:noRegion></affiliation></author><author><name sortKey="Kamitani, Wataru" sort="Kamitani, Wataru" uniqKey="Kamitani W" first="Wataru" last="Kamitani">Wataru Kamitani</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Global COE Program, Research Institute for Microbial Diseases, Osaka University</s1><s2>Osaka</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Japon</country><wicri:noRegion>Osaka</wicri:noRegion></affiliation></author><author><name sortKey="Dediego, Marta L" sort="Dediego, Marta L" uniqKey="Dediego M" first="Marta L." last="Dediego">Marta L. Dediego</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Department of Molecular and Cell Biology, Centro Nacional de Biotecnologia (CNB-CSIC), Campus Universidad Autonoma</s1><s2>Madrid</s2><s3>ESP</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Espagne</country><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author><author><name sortKey="Enjuanes, Luis" sort="Enjuanes, Luis" uniqKey="Enjuanes L" first="Luis" last="Enjuanes">Luis Enjuanes</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Department of Molecular and Cell Biology, Centro Nacional de Biotecnologia (CNB-CSIC), Campus Universidad Autonoma</s1><s2>Madrid</s2><s3>ESP</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Espagne</country><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author><author><name sortKey="Matsuura, Yoshiharu" sort="Matsuura, Yoshiharu" uniqKey="Matsuura Y" first="Yoshiharu" last="Matsuura">Yoshiharu Matsuura</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University</s1><s2>Osaka</s2><s3>JPN</s3><sZ>5 aut.</sZ></inist:fA14><country>Japon</country><wicri:noRegion>Osaka</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Coronavirus</term><term>Genetic translation</term><term>Messenger RNA</term><term>Severe acute respiratory syndrome</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term><term>Traduction génétique</term><term>RNA messager</term><term>Syndrome respiratoire aigu sévère</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) coronavirus (SCoV) is an enveloped virus containing a single-stranded, positive-sense RNA genome. Nine mRNAs carrying a set of common 5' and 3' untranslated regions (UTR) are synthesized from the incoming viral genomic RNA in cells infected with SCoV. A nonstructural SCoV nsp1 protein causes a severe translational shutoff by binding to the 40S ribosomal subunits. The nsp1-40S ribosome complex further induces an endonucleolytic cleavage near the 5'UTR of host mRNA. However, the mechanism by which SCoV viral proteins are efficiently produced in infected cells in which host protein synthesis is impaired by nsp is unknown. In this study, we investigated the role of the viral UTRs in evasion of the nsp1-mediated shutoff. Luciferase activities were significantly suppressed in cells expressing nsp1 together with the mRNA carrying a luciferase gene, while nsp1 failed to suppress luciferase activities of the mRNA flanked by the 5'UTR of SCoV. An RNA-protein binding assay and RNA decay assay revealed that nsp1 bound to stem-loop 1 (SL1) in the 5'UTR of SCoV RNA and that the specific interaction with nsp1 stabilized the mRNA carrying SL1. Furthermore, experiments using an SCoV replicon system showed that the specific interaction enhanced the SCoV replication. The specific interaction of nsp1 with SL1 is an important strategy to facilitate efficient viral gene expression in infected cells, in which nsp1 suppresses host gene expression. 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All rights reserved.</s1></fA44><fA45><s0>40 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>12-0390363</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of virology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Severe acute respiratory syndrome (SARS) coronavirus (SCoV) is an enveloped virus containing a single-stranded, positive-sense RNA genome. Nine mRNAs carrying a set of common 5' and 3' untranslated regions (UTR) are synthesized from the incoming viral genomic RNA in cells infected with SCoV. A nonstructural SCoV nsp1 protein causes a severe translational shutoff by binding to the 40S ribosomal subunits. The nsp1-40S ribosome complex further induces an endonucleolytic cleavage near the 5'UTR of host mRNA. However, the mechanism by which SCoV viral proteins are efficiently produced in infected cells in which host protein synthesis is impaired by nsp is unknown. In this study, we investigated the role of the viral UTRs in evasion of the nsp1-mediated shutoff. Luciferase activities were significantly suppressed in cells expressing nsp1 together with the mRNA carrying a luciferase gene, while nsp1 failed to suppress luciferase activities of the mRNA flanked by the 5'UTR of SCoV. An RNA-protein binding assay and RNA decay assay revealed that nsp1 bound to stem-loop 1 (SL1) in the 5'UTR of SCoV RNA and that the specific interaction with nsp1 stabilized the mRNA carrying SL1. Furthermore, experiments using an SCoV replicon system showed that the specific interaction enhanced the SCoV replication. The specific interaction of nsp1 with SL1 is an important strategy to facilitate efficient viral gene expression in infected cells, in which nsp1 suppresses host gene expression. 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Dediego</name></region><name sortKey="Enjuanes, Luis" sort="Enjuanes, Luis" uniqKey="Enjuanes L" first="Luis" last="Enjuanes">Luis Enjuanes</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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