A Yeast Suppressor Screen Used To Identify Mammalian SIRT1 as a Proviral Factor for Middle East Respiratory Syndrome Coronavirus Replication.
Identifieur interne : 000517 ( PubMed/Curation ); précédent : 000516; suivant : 000518A Yeast Suppressor Screen Used To Identify Mammalian SIRT1 as a Proviral Factor for Middle East Respiratory Syndrome Coronavirus Replication.
Auteurs : Stuart Weston [États-Unis] ; Krystal L. Matthews [États-Unis] ; Rachel Lent [États-Unis] ; Alexandra Vlk [États-Unis] ; Rob Haupt [États-Unis] ; Tami Kingsbury [États-Unis] ; Matthew B. Frieman [États-Unis]Source :
- Journal of virology [ 1098-5514 ] ; 2019.
Abstract
Viral proteins must intimately interact with the host cell machinery during virus replication. Here, we used the yeast Saccharomyces cerevisiae as a system to identify novel functional interactions between viral proteins and eukaryotic cells. Our work demonstrates that when the Middle East respiratory syndrome coronavirus (MERS-CoV) ORF4a accessory gene is expressed in yeast it causes a slow-growth phenotype. ORF4a has been characterized as an interferon antagonist in mammalian cells, and yet yeast lack an interferon system, suggesting further interactions between ORF4a and eukaryotic cells. Using the slow-growth phenotype as a reporter of ORF4a function, we utilized the yeast knockout library collection to perform a suppressor screen where we identified the YDL042C/SIR2 yeast gene as a suppressor of ORF4a function. The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase. We found that when SIRT1 was inhibited by either chemical or genetic manipulation, there was reduced MERS-CoV replication, suggesting that SIRT1 is a proviral factor for MERS-CoV. Moreover, ORF4a inhibited SIRT1-mediated modulation of NF-κB signaling, demonstrating a functional link between ORF4a and SIRT1 in mammalian cells. Overall, the data presented here demonstrate the utility of yeast studies for identifying genetic interactions between viral proteins and eukaryotic cells. We also demonstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and that ORF4a has a role in modulating its activity in cells.IMPORTANCE Middle East respiratory syndrome coronavirus (MERS-CoV) initially emerged in 2012 and has since been responsible for over 2,300 infections, with a case fatality ratio of approximately 35%. We have used the highly characterized model system of Saccharomyces cerevisiae to investigate novel functional interactions between viral proteins and eukaryotic cells that may provide new avenues for antiviral intervention. We identify a functional link between the MERS-CoV ORF4a proteins and the YDL042C/SIR2 yeast gene. The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase. We demonstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and that ORF4a has a role in modulating its activity in mammalian cells.
DOI: 10.1128/JVI.00197-19
PubMed: 31142674
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Matthews</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Lent, Rachel" sort="Lent, Rachel" uniqKey="Lent R" first="Rachel" last="Lent">Rachel Lent</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Vlk, Alexandra" sort="Vlk, Alexandra" uniqKey="Vlk A" first="Alexandra" last="Vlk">Alexandra Vlk</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Haupt, Rob" sort="Haupt, Rob" uniqKey="Haupt R" first="Rob" last="Haupt">Rob Haupt</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Kingsbury, Tami" sort="Kingsbury, Tami" uniqKey="Kingsbury T" first="Tami" last="Kingsbury">Tami Kingsbury</name><affiliation wicri:level="1"><nlm:affiliation>Center for Stem Cell Biology and Regenerative Medicine, Marlene and Stewart Greenebaum Cancer Center, Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Stem Cell Biology and Regenerative Medicine, Marlene and Stewart Greenebaum Cancer Center, Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea></affiliation></author><author><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B" last="Frieman">Matthew B. Frieman</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA MFrieman@som.umaryland.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland</wicri:regionArea></affiliation></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Viral proteins must intimately interact with the host cell machinery during virus replication. Here, we used the yeast <i>Saccharomyces cerevisiae</i> as a system to identify novel functional interactions between viral proteins and eukaryotic cells. Our work demonstrates that when the Middle East respiratory syndrome coronavirus (MERS-CoV) ORF4a accessory gene is expressed in yeast it causes a slow-growth phenotype. ORF4a has been characterized as an interferon antagonist in mammalian cells, and yet yeast lack an interferon system, suggesting further interactions between ORF4a and eukaryotic cells. Using the slow-growth phenotype as a reporter of ORF4a function, we utilized the yeast knockout library collection to perform a suppressor screen where we identified the YDL042C/SIR2 yeast gene as a suppressor of ORF4a function. The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase. We found that when SIRT1 was inhibited by either chemical or genetic manipulation, there was reduced MERS-CoV replication, suggesting that SIRT1 is a proviral factor for MERS-CoV. Moreover, ORF4a inhibited SIRT1-mediated modulation of NF-κB signaling, demonstrating a functional link between ORF4a and SIRT1 in mammalian cells. Overall, the data presented here demonstrate the utility of yeast studies for identifying genetic interactions between viral proteins and eukaryotic cells. We also demonstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and that ORF4a has a role in modulating its activity in cells.<b>IMPORTANCE</b> Middle East respiratory syndrome coronavirus (MERS-CoV) initially emerged in 2012 and has since been responsible for over 2,300 infections, with a case fatality ratio of approximately 35%. We have used the highly characterized model system of <i>Saccharomyces cerevisiae</i> to investigate novel functional interactions between viral proteins and eukaryotic cells that may provide new avenues for antiviral intervention. We identify a functional link between the MERS-CoV ORF4a proteins and the YDL042C/SIR2 yeast gene. The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase. We demonstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and that ORF4a has a role in modulating its activity in mammalian cells.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">31142674</PMID><DateRevised><Year>2020</Year><Month>02</Month><Day>25</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>93</Volume><Issue>16</Issue><PubDate><Year>2019</Year><Month>Aug</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>A Yeast Suppressor Screen Used To Identify Mammalian SIRT1 as a Proviral Factor for Middle East Respiratory Syndrome Coronavirus Replication.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e00197-19</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.00197-19</ELocationID><Abstract><AbstractText>Viral proteins must intimately interact with the host cell machinery during virus replication. Here, we used the yeast <i>Saccharomyces cerevisiae</i> as a system to identify novel functional interactions between viral proteins and eukaryotic cells. Our work demonstrates that when the Middle East respiratory syndrome coronavirus (MERS-CoV) ORF4a accessory gene is expressed in yeast it causes a slow-growth phenotype. ORF4a has been characterized as an interferon antagonist in mammalian cells, and yet yeast lack an interferon system, suggesting further interactions between ORF4a and eukaryotic cells. Using the slow-growth phenotype as a reporter of ORF4a function, we utilized the yeast knockout library collection to perform a suppressor screen where we identified the YDL042C/SIR2 yeast gene as a suppressor of ORF4a function. The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase. We found that when SIRT1 was inhibited by either chemical or genetic manipulation, there was reduced MERS-CoV replication, suggesting that SIRT1 is a proviral factor for MERS-CoV. Moreover, ORF4a inhibited SIRT1-mediated modulation of NF-κB signaling, demonstrating a functional link between ORF4a and SIRT1 in mammalian cells. Overall, the data presented here demonstrate the utility of yeast studies for identifying genetic interactions between viral proteins and eukaryotic cells. We also demonstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and that ORF4a has a role in modulating its activity in cells.<b>IMPORTANCE</b> Middle East respiratory syndrome coronavirus (MERS-CoV) initially emerged in 2012 and has since been responsible for over 2,300 infections, with a case fatality ratio of approximately 35%. We have used the highly characterized model system of <i>Saccharomyces cerevisiae</i> to investigate novel functional interactions between viral proteins and eukaryotic cells that may provide new avenues for antiviral intervention. We identify a functional link between the MERS-CoV ORF4a proteins and the YDL042C/SIR2 yeast gene. The mammalian homologue of SIR2 is SIRT1, an NAD-dependent histone deacetylase. We demonstrate for the first time that SIRT1 is a proviral factor for MERS-CoV replication and that ORF4a has a role in modulating its activity in mammalian cells.</AbstractText><CopyrightInformation>Copyright © 2019 American Society for Microbiology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Weston</LastName><ForeName>Stuart</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matthews</LastName><ForeName>Krystal L</ForeName><Initials>KL</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lent</LastName><ForeName>Rachel</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vlk</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Haupt</LastName><ForeName>Rob</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kingsbury</LastName><ForeName>Tami</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Center for Stem Cell Biology and Regenerative Medicine, Marlene and Stewart Greenebaum Cancer Center, Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frieman</LastName><ForeName>Matthew B</ForeName><Initials>MB</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA MFrieman@som.umaryland.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>07</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">MERS-CoV</Keyword><Keyword MajorTopicYN="N">ORF4a</Keyword><Keyword MajorTopicYN="N">SIRT1</Keyword><Keyword MajorTopicYN="N">host-virus interaction</Keyword><Keyword MajorTopicYN="N">suppressor screen</Keyword><Keyword MajorTopicYN="N">virus-host interaction</Keyword><Keyword MajorTopicYN="N">yeast</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>02</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>05</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>5</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>5</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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