Expression of authentic vaccinia virus-specific and inserted viral and cellular genes under control of an early vaccinia virus promoter is regulated post-transcriptionally in interferon-treated chick embryo fibroblasts
Identifieur interne : 001595 ( Istex/Corpus ); précédent : 001594; suivant : 001596Expression of authentic vaccinia virus-specific and inserted viral and cellular genes under control of an early vaccinia virus promoter is regulated post-transcriptionally in interferon-treated chick embryo fibroblasts
Auteurs : Hans Joachim Degen ; Doris Blum ; Joachim Grün ; Christoph JungwirthSource :
- Virology [ 0042-6822 ] ; 1992.
English descriptors
- Teeft :
- Academic press, Additional mechanism, Bodo, Chick, Chick embryo fibroblasts, Chloride method, Control cells, Cytosine arabinoside, Different inhibitors, Different protocols, Different times, Embryo, Experimental conditions, Fibroblast, Foreign genes, Gene, Gene expression, Grun, Histone, Human histone, Hybridization, Influenza, Influenza virus, Interferon, Interferon sensitivity, Interferon treatment, Jungwirth, Liquid scintillation, Mdbk, Mdbk cells, Mrna, Mrna synthesis, Northern blot analysis, Pretreated, Pretreatment, Promoter, Protein synthesis, Reaction mixtures, Scintillation, Vaccinia, Vaccinia virus, Vaccinia virus genome, Vaccinia virus promoter, Various genes, Viral, Viral mrna, Viral mrnas, Viral protein synthesis, Virology, Virus.
Abstract
Abstract: The interferon sensitivity of the expression of an influenza-virus hemagglutinin (HA) gene cloned into the thymidine kinase (TK) gene of vaccinia virus was studied in chick embryo fibroblasts (CEF) and Madin-Darby bovine kidney (MDBK) cells. In CEF, the expression of the HA gene is inhibited by pretreatment of cells with homologous interferon. In MDBK cells, on the other hand, expression of the HA is not impaired by pretreatment with human interferon-α, and the synthesis of early vaccinia virus enzymes was also unaffected. These results indicate that the interferon sensitivity of HA gene expression is at least in part controlled by flanking regions of vaccinia virus DNA. In this report, we also address the question whether the expression of an influenza virus HA gene and the human histone H1° gene under control of a vaccinia virus immediate early promoter is affected in interferon-treated CEF by a post-transcriptional mechanism in the same way as the expression of the viral TK gene. In interferon-treated cells mRNA synthesis specific for all these genes was enhanced. Steady state mRNA levels 6 hr p.i. were, however, lower than the amounts expected from the rate of mRNA synthesis during the first 6 hr p.i., suggesting that part of the viral RNA was degraded. Degradation resistant mRNA accumulated in the interferon-treated cells in an amount comparable to that found in infected CEF. This RNA could be translated into viral protein in a cell-free system. Therefore the degradation of viral mRNA cannot solely be responsible for the inhibition of viral protein synthesis in interferon-treated cells.
Url:
DOI: 10.1016/0042-6822(92)90740-G
Links to Exploration step
ISTEX:2CA10B4F54E23E6B97A7D0BA3779B316C45ADD8ELe document en format XML
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sensitivity</term><term>Interferon treatment</term><term>Jungwirth</term><term>Liquid scintillation</term><term>Mdbk</term><term>Mdbk cells</term><term>Mrna</term><term>Mrna synthesis</term><term>Northern blot analysis</term><term>Pretreated</term><term>Pretreatment</term><term>Promoter</term><term>Protein synthesis</term><term>Reaction mixtures</term><term>Scintillation</term><term>Vaccinia</term><term>Vaccinia virus</term><term>Vaccinia virus genome</term><term>Vaccinia virus promoter</term><term>Various genes</term><term>Viral</term><term>Viral mrna</term><term>Viral mrnas</term><term>Viral protein synthesis</term><term>Virology</term><term>Virus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The interferon sensitivity of the expression of an influenza-virus hemagglutinin (HA) gene cloned into the thymidine kinase (TK) gene of vaccinia virus was studied in chick embryo fibroblasts (CEF) and Madin-Darby bovine kidney (MDBK) cells. In CEF, the expression of the HA gene is inhibited by pretreatment of cells with homologous interferon. In MDBK cells, on the other hand, expression of the HA is not impaired by pretreatment with human interferon-α, and the synthesis of early vaccinia virus enzymes was also unaffected. These results indicate that the interferon sensitivity of HA gene expression is at least in part controlled by flanking regions of vaccinia virus DNA. In this report, we also address the question whether the expression of an influenza virus HA gene and the human histone H1° gene under control of a vaccinia virus immediate early promoter is affected in interferon-treated CEF by a post-transcriptional mechanism in the same way as the expression of the viral TK gene. In interferon-treated cells mRNA synthesis specific for all these genes was enhanced. Steady state mRNA levels 6 hr p.i. were, however, lower than the amounts expected from the rate of mRNA synthesis during the first 6 hr p.i., suggesting that part of the viral RNA was degraded. Degradation resistant mRNA accumulated in the interferon-treated cells in an amount comparable to that found in infected CEF. This RNA could be translated into viral protein in a cell-free system. 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In CEF, the expression of the HA gene is inhibited by pretreatment of cells with homologous interferon. In MDBK cells, on the other hand, expression of the HA is not impaired by pretreatment with human interferon-α, and the synthesis of early vaccinia virus enzymes was also unaffected. These results indicate that the interferon sensitivity of HA gene expression is at least in part controlled by flanking regions of vaccinia virus DNA. In this report, we also address the question whether the expression of an influenza virus HA gene and the human histone H1° gene under control of a vaccinia virus immediate early promoter is affected in interferon-treated CEF by a post-transcriptional mechanism in the same way as the expression of the viral TK gene. In interferon-treated cells mRNA synthesis specific for all these genes was enhanced. Steady state mRNA levels 6 hr p.i. were, however, lower than the amounts expected from the rate of mRNA synthesis during the first 6 hr p.i., suggesting that part of the viral RNA was degraded. Degradation resistant mRNA accumulated in the interferon-treated cells in an amount comparable to that found in infected CEF. This RNA could be translated into viral protein in a cell-free system. Therefore the degradation of viral mRNA cannot solely be responsible for the inhibition of viral protein synthesis in interferon-treated cells.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>257</abstractWordCount><abstractCharCount>1628</abstractCharCount><keywordCount>0</keywordCount><score>9.735</score><pdfWordCount>4735</pdfWordCount><pdfCharCount>34717</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>612 x 792 pts (letter)</pdfPageSize></qualityIndicators><title>Expression of authentic vaccinia virus-specific and inserted viral and cellular genes under control of an early vaccinia virus promoter is regulated post-transcriptionally in interferon-treated chick embryo fibroblasts</title><pmid><json:string>1373550</json:string></pmid><pii><json:string>0042-6822(92)90740-G</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Natl. Acad. Sci. 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Gething</json:string><json:string>B. Moss</json:string><json:string>In</json:string><json:string>I. Redmann-Moller</json:string><json:string>H. Kriesinger</json:string><json:string>C. Stoppe</json:string><json:string>C. Phillips</json:string></persName><placeName><json:string>Naundorf</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Ransohoff et al., 1985</json:string><json:string>Doenecke and Tonjes, 1985</json:string><json:string>Samuel and Brody, 1990</json:string><json:string>GrOn et al., 1991</json:string><json:string>Dowling and Youngner, 1983, 1986</json:string><json:string>Gething et al., 1980</json:string><json:string>Joklik, 1962</json:string><json:string>Hruby et al., 1980</json:string><json:string>Secher, 1981</json:string><json:string>Joklik and Merigan, 1966</json:string><json:string>Grun et al., 1991</json:string><json:string>Thomas, 1983</json:string><json:string>Thacore and Youngner, 1973</json:string><json:string>Kessler, 1981</json:string><json:string>Rigby, 1977</json:string><json:string>Rossman and Vilcek, 1969</json:string><json:string>Franke et al., 1985</json:string><json:string>Hruby and Ball, 1982</json:string><json:string>Kaufmann and Murtha, 1987</json:string><json:string>Bodo and Jungwirth, 1967</json:string><json:string>Laemmli, 1970</json:string><json:string>Bajszar et al., 1983</json:string><json:string>Strube et al., 1985</json:string><json:string>Wittek et al. (1980)</json:string><json:string>Jungwirth et al., 1972</json:string><json:string>Chirgwin et al., 1979</json:string><json:string>Jungwirth et al., 1977</json:string><json:string>Smith et al., 1983</json:string><json:string>Grun et al., 1987a, 1991</json:string><json:string>Grun et al., 1987a,b</json:string><json:string>Grijn et al., 1987a</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-GXXKMM4F-N</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - 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In CEF, the expression of the HA gene is inhibited by pretreatment of cells with homologous interferon. In MDBK cells, on the other hand, expression of the HA is not impaired by pretreatment with human interferon-α, and the synthesis of early vaccinia virus enzymes was also unaffected. These results indicate that the interferon sensitivity of HA gene expression is at least in part controlled by flanking regions of vaccinia virus DNA. In this report, we also address the question whether the expression of an influenza virus HA gene and the human histone H1° gene under control of a vaccinia virus immediate early promoter is affected in interferon-treated CEF by a post-transcriptional mechanism in the same way as the expression of the viral TK gene. In interferon-treated cells mRNA synthesis specific for all these genes was enhanced. Steady state mRNA levels 6 hr p.i. were, however, lower than the amounts expected from the rate of mRNA synthesis during the first 6 hr p.i., suggesting that part of the viral RNA was degraded. Degradation resistant mRNA accumulated in the interferon-treated cells in an amount comparable to that found in infected CEF. This RNA could be translated into viral protein in a cell-free system. Therefore the degradation of viral mRNA cannot solely be responsible for the inhibition of viral protein synthesis in interferon-treated cells.</p></abstract></profileDesc><revisionDesc><change when="1992">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-GXXKMM4F-N/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YVIRO</jid><aid>9290740G</aid><ce:pii>0042-6822(92)90740-G</ce:pii><ce:doi>10.1016/0042-6822(92)90740-G</ce:doi><ce:copyright type="unknown" year="1992"></ce:copyright></item-info><head><ce:title>Expression of authentic vaccinia virus-specific and inserted viral and cellular genes under control of an early vaccinia virus promoter is regulated post-transcriptionally in interferon-treated chick embryo fibroblasts</ce:title><ce:author-group><ce:author><ce:given-name>Hans Joachim</ce:given-name><ce:surname>Degen</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Doris</ce:given-name><ce:surname>Blum</ce:surname></ce:author><ce:author><ce:given-name>Joachim</ce:given-name><ce:surname>Grün</ce:surname></ce:author><ce:author><ce:given-name>Christoph</ce:given-name><ce:surname>Jungwirth</ce:surname></ce:author><ce:affiliation><ce:textfn>Institute of Virology and Immunobiology, University of Würzburg, Versbacher Strasse 7, D-8700 Würzburg, Germany</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>To whom reprint requests should be addressed.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="29" month="7" year="1991"></ce:date-received><ce:date-accepted day="2" month="1" year="1992"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The interferon sensitivity of the expression of an influenza-virus hemagglutinin (HA) gene cloned into the thymidine kinase (TK) gene of vaccinia virus was studied in chick embryo fibroblasts (CEF) and Madin-Darby bovine kidney (MDBK) cells. In CEF, the expression of the HA gene is inhibited by pretreatment of cells with homologous interferon. In MDBK cells, on the other hand, expression of the HA is not impaired by pretreatment with human interferon-α, and the synthesis of early vaccinia virus enzymes was also unaffected. These results indicate that the interferon sensitivity of HA gene expression is at least in part controlled by flanking regions of vaccinia virus DNA. In this report, we also address the question whether the expression of an influenza virus HA gene and the human histone H1° gene under control of a vaccinia virus immediate early promoter is affected in interferon-treated CEF by a post-transcriptional mechanism in the same way as the expression of the viral TK gene. In interferon-treated cells mRNA synthesis specific for all these genes was enhanced. Steady state mRNA levels 6 hr p.i. were, however, lower than the amounts expected from the rate of mRNA synthesis during the first 6 hr p.i., suggesting that part of the viral RNA was degraded. Degradation resistant mRNA accumulated in the interferon-treated cells in an amount comparable to that found in infected CEF. This RNA could be translated into viral protein in a cell-free system. Therefore the degradation of viral mRNA cannot solely be responsible for the inhibition of viral protein synthesis in interferon-treated cells.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Expression of authentic vaccinia virus-specific and inserted viral and cellular genes under control of an early vaccinia virus promoter is regulated post-transcriptionally in interferon-treated chick embryo fibroblasts</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Expression of authentic vaccinia virus-specific and inserted viral and cellular genes under control of an early vaccinia virus promoter is regulated post-transcriptionally in interferon-treated chick embryo fibroblasts</title></titleInfo><name type="personal"><namePart type="given">Hans Joachim</namePart><namePart type="family">Degen</namePart><affiliation>Institute of Virology and Immunobiology, University of Würzburg, Versbacher Strasse 7, D-8700 Würzburg, Germany</affiliation><description>To whom reprint requests should be addressed.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Doris</namePart><namePart type="family">Blum</namePart><affiliation>Institute of Virology and Immunobiology, University of Würzburg, Versbacher Strasse 7, D-8700 Würzburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joachim</namePart><namePart type="family">Grün</namePart><affiliation>Institute of Virology and Immunobiology, University of Würzburg, Versbacher Strasse 7, D-8700 Würzburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christoph</namePart><namePart type="family">Jungwirth</namePart><affiliation>Institute of Virology and Immunobiology, University of Würzburg, Versbacher Strasse 7, D-8700 Würzburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1992</dateIssued><copyrightDate encoding="w3cdtf">1992</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: The interferon sensitivity of the expression of an influenza-virus hemagglutinin (HA) gene cloned into the thymidine kinase (TK) gene of vaccinia virus was studied in chick embryo fibroblasts (CEF) and Madin-Darby bovine kidney (MDBK) cells. In CEF, the expression of the HA gene is inhibited by pretreatment of cells with homologous interferon. In MDBK cells, on the other hand, expression of the HA is not impaired by pretreatment with human interferon-α, and the synthesis of early vaccinia virus enzymes was also unaffected. These results indicate that the interferon sensitivity of HA gene expression is at least in part controlled by flanking regions of vaccinia virus DNA. In this report, we also address the question whether the expression of an influenza virus HA gene and the human histone H1° gene under control of a vaccinia virus immediate early promoter is affected in interferon-treated CEF by a post-transcriptional mechanism in the same way as the expression of the viral TK gene. In interferon-treated cells mRNA synthesis specific for all these genes was enhanced. Steady state mRNA levels 6 hr p.i. were, however, lower than the amounts expected from the rate of mRNA synthesis during the first 6 hr p.i., suggesting that part of the viral RNA was degraded. Degradation resistant mRNA accumulated in the interferon-treated cells in an amount comparable to that found in infected CEF. This RNA could be translated into viral protein in a cell-free system. Therefore the degradation of viral mRNA cannot solely be responsible for the inhibition of viral protein synthesis in interferon-treated cells.</abstract><relatedItem type="host"><titleInfo><title>Virology</title></titleInfo><titleInfo type="abbreviated"><title>YVIRO</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1992</dateIssued></originInfo><identifier type="ISSN">0042-6822</identifier><identifier type="PII">S0042-6822(00)X0381-9</identifier><part><date>1992</date><detail type="volume"><number>188</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>416</end></extent><extent unit="pages"><start>114</start><end>121</end></extent></part></relatedItem><identifier type="istex">2CA10B4F54E23E6B97A7D0BA3779B316C45ADD8E</identifier><identifier type="ark">ark:/67375/6H6-GXXKMM4F-N</identifier><identifier type="DOI">10.1016/0042-6822(92)90740-G</identifier><identifier type="PII">0042-6822(92)90740-G</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-GXXKMM4F-N/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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