Inactivation of hepatitis C virus cDNA transgene by hypermethylation in transgenic mice
Transgenic mice were produced by microinjection of a partial hepatitis C virus (HCV) genome sequence including the structural protein region, under the control of the albumin promoter and enhancer into fertilized eggs of C57BL/6 and BDF1 mice. Three founders carrying at least five copies of the tran...
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| Veröffentlicht in: | Archives of virology 1996, Vol.141 (5), p.951-958 |
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| container_title | Archives of virology |
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| creator | KATO, T AHMED, M ESUMI, M YAMAMOTO, T TAKAHASHI, H OOHARA, M IKEDA, T AIDA, Y KATSUKI, M ARAKAWA, Y SHIKATA, T |
| description | Transgenic mice were produced by microinjection of a partial hepatitis C virus (HCV) genome sequence including the structural protein region, under the control of the albumin promoter and enhancer into fertilized eggs of C57BL/6 and BDF1 mice. Three founders carrying at least five copies of the transgene but not expressing HCV-specific RNA were generated. Methylation analysis indicated that the transgene was extensively methylated. Mapping of methylated cytosine residues of the transgenic mouse DNA showed that all C residues of a particular part of the HCV genome but not all the CpG island like sequences were methylated. Transiently expressed HCV cDNA in COS7 cells and the active endogenous albumin gene were not methylated. Furthermore, 5-azacytidine, a potent demethylating agent, induced HCV gene expression in a line of these transgenic mice. These results suggest that methylation of HCV cDNA is a cause of its inactive expression in transgenic mice, and that this phenomenon may occur in other stable systems for expression of the HCV genome. |
| doi_str_mv | 10.1007/BF01718169 |
| format | Article |
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Three founders carrying at least five copies of the transgene but not expressing HCV-specific RNA were generated. Methylation analysis indicated that the transgene was extensively methylated. Mapping of methylated cytosine residues of the transgenic mouse DNA showed that all C residues of a particular part of the HCV genome but not all the CpG island like sequences were methylated. Transiently expressed HCV cDNA in COS7 cells and the active endogenous albumin gene were not methylated. Furthermore, 5-azacytidine, a potent demethylating agent, induced HCV gene expression in a line of these transgenic mice. These results suggest that methylation of HCV cDNA is a cause of its inactive expression in transgenic mice, and that this phenomenon may occur in other stable systems for expression of the HCV genome.</description><identifier>ISSN: 0304-8608</identifier><identifier>EISSN: 1432-8798</identifier><identifier>DOI: 10.1007/BF01718169</identifier><identifier>PMID: 8678840</identifier><language>eng</language><publisher>Wien: Springer</publisher><subject>Animals ; Base Sequence ; Biological and medical sciences ; DNA, Complementary - metabolism ; DNA, Viral - genetics ; Fundamental and applied biological sciences. Psychology ; Genetics ; Hepacivirus - genetics ; hepatitis C virus ; Methylation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microbiology ; Molecular Sequence Data ; Transgenes ; Virology</subject><ispartof>Archives of virology, 1996, Vol.141 (5), p.951-958</ispartof><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c257t-dbca498d8a35fd9c0ba34cc565a9d9ba5a3f5983da42c1fb3140dc48dbf0ad9c3</citedby><cites>FETCH-LOGICAL-c257t-dbca498d8a35fd9c0ba34cc565a9d9ba5a3f5983da42c1fb3140dc48dbf0ad9c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3101335$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8678840$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KATO, T</creatorcontrib><creatorcontrib>AHMED, M</creatorcontrib><creatorcontrib>ESUMI, M</creatorcontrib><creatorcontrib>YAMAMOTO, T</creatorcontrib><creatorcontrib>TAKAHASHI, H</creatorcontrib><creatorcontrib>OOHARA, M</creatorcontrib><creatorcontrib>IKEDA, T</creatorcontrib><creatorcontrib>AIDA, Y</creatorcontrib><creatorcontrib>KATSUKI, M</creatorcontrib><creatorcontrib>ARAKAWA, Y</creatorcontrib><creatorcontrib>SHIKATA, T</creatorcontrib><title>Inactivation of hepatitis C virus cDNA transgene by hypermethylation in transgenic mice</title><title>Archives of virology</title><addtitle>Arch Virol</addtitle><description>Transgenic mice were produced by microinjection of a partial hepatitis C virus (HCV) genome sequence including the structural protein region, under the control of the albumin promoter and enhancer into fertilized eggs of C57BL/6 and BDF1 mice. Three founders carrying at least five copies of the transgene but not expressing HCV-specific RNA were generated. Methylation analysis indicated that the transgene was extensively methylated. Mapping of methylated cytosine residues of the transgenic mouse DNA showed that all C residues of a particular part of the HCV genome but not all the CpG island like sequences were methylated. Transiently expressed HCV cDNA in COS7 cells and the active endogenous albumin gene were not methylated. Furthermore, 5-azacytidine, a potent demethylating agent, induced HCV gene expression in a line of these transgenic mice. These results suggest that methylation of HCV cDNA is a cause of its inactive expression in transgenic mice, and that this phenomenon may occur in other stable systems for expression of the HCV genome.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>DNA, Complementary - metabolism</subject><subject>DNA, Viral - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetics</subject><subject>Hepacivirus - genetics</subject><subject>hepatitis C virus</subject><subject>Methylation</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Microbiology</subject><subject>Molecular Sequence Data</subject><subject>Transgenes</subject><subject>Virology</subject><issn>0304-8608</issn><issn>1432-8798</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkDtPwzAURi0EKqWwsCN5QAxIATu2Y3uEQqFSBQuIMXL8oEZ5FDuplH9PUKMyMt2r-537DQeAc4xuMEL89n6BMMcCZ_IATDElaSK4FIdgigiiiciQOAYnMX4hNBwIm4CJyLgQFE3Bx7JWuvVb1fqmho2Da7sZ9tZHOIdbH7oI9cPLHWyDquOnrS0serjuNzZUtl335e7P13vAa1h5bU_BkVNltGfjnIH3xePb_DlZvT4t53erRKeMt4kptKJSGKEIc0ZqVChCtWYZU9LIQjFFHJOCGEVTjV1BMEVGU2EKh9TAkxm42vVuQvPd2djmlY_alqWqbdPFnAuMecqzf0HMJEo5pQN4vQN1aGIM1uWb4CsV-hyj_Fd3_qd7gC_G1q6orNmjo98hvxxzFbUq3SBJ-7jHCEaYEEZ-APAmh_s</recordid><startdate>1996</startdate><enddate>1996</enddate><creator>KATO, T</creator><creator>AHMED, M</creator><creator>ESUMI, M</creator><creator>YAMAMOTO, T</creator><creator>TAKAHASHI, H</creator><creator>OOHARA, M</creator><creator>IKEDA, T</creator><creator>AIDA, Y</creator><creator>KATSUKI, M</creator><creator>ARAKAWA, Y</creator><creator>SHIKATA, T</creator><general>Springer</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>1996</creationdate><title>Inactivation of hepatitis C virus cDNA transgene by hypermethylation in transgenic mice</title><author>KATO, T ; AHMED, M ; ESUMI, M ; YAMAMOTO, T ; TAKAHASHI, H ; OOHARA, M ; IKEDA, T ; AIDA, Y ; KATSUKI, M ; ARAKAWA, Y ; SHIKATA, T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c257t-dbca498d8a35fd9c0ba34cc565a9d9ba5a3f5983da42c1fb3140dc48dbf0ad9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>DNA, Complementary - metabolism</topic><topic>DNA, Viral - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetics</topic><topic>Hepacivirus - genetics</topic><topic>hepatitis C virus</topic><topic>Methylation</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Microbiology</topic><topic>Molecular Sequence Data</topic><topic>Transgenes</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KATO, T</creatorcontrib><creatorcontrib>AHMED, M</creatorcontrib><creatorcontrib>ESUMI, M</creatorcontrib><creatorcontrib>YAMAMOTO, T</creatorcontrib><creatorcontrib>TAKAHASHI, H</creatorcontrib><creatorcontrib>OOHARA, M</creatorcontrib><creatorcontrib>IKEDA, T</creatorcontrib><creatorcontrib>AIDA, Y</creatorcontrib><creatorcontrib>KATSUKI, M</creatorcontrib><creatorcontrib>ARAKAWA, Y</creatorcontrib><creatorcontrib>SHIKATA, T</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KATO, T</au><au>AHMED, M</au><au>ESUMI, M</au><au>YAMAMOTO, T</au><au>TAKAHASHI, H</au><au>OOHARA, M</au><au>IKEDA, T</au><au>AIDA, Y</au><au>KATSUKI, M</au><au>ARAKAWA, Y</au><au>SHIKATA, T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inactivation of hepatitis C virus cDNA transgene by hypermethylation in transgenic mice</atitle><jtitle>Archives of virology</jtitle><addtitle>Arch Virol</addtitle><date>1996</date><risdate>1996</risdate><volume>141</volume><issue>5</issue><spage>951</spage><epage>958</epage><pages>951-958</pages><issn>0304-8608</issn><eissn>1432-8798</eissn><abstract>Transgenic mice were produced by microinjection of a partial hepatitis C virus (HCV) genome sequence including the structural protein region, under the control of the albumin promoter and enhancer into fertilized eggs of C57BL/6 and BDF1 mice. Three founders carrying at least five copies of the transgene but not expressing HCV-specific RNA were generated. Methylation analysis indicated that the transgene was extensively methylated. Mapping of methylated cytosine residues of the transgenic mouse DNA showed that all C residues of a particular part of the HCV genome but not all the CpG island like sequences were methylated. Transiently expressed HCV cDNA in COS7 cells and the active endogenous albumin gene were not methylated. Furthermore, 5-azacytidine, a potent demethylating agent, induced HCV gene expression in a line of these transgenic mice. These results suggest that methylation of HCV cDNA is a cause of its inactive expression in transgenic mice, and that this phenomenon may occur in other stable systems for expression of the HCV genome.</abstract><cop>Wien</cop><cop>New York, NY</cop><pub>Springer</pub><pmid>8678840</pmid><doi>10.1007/BF01718169</doi><tpages>8</tpages></addata></record> |
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| ispartof | Archives of virology, 1996, Vol.141 (5), p.951-958 |
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| language | eng |
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| source | MEDLINE; SpringerNature Complete Journals |
| subjects | Animals Base Sequence Biological and medical sciences DNA, Complementary - metabolism DNA, Viral - genetics Fundamental and applied biological sciences. Psychology Genetics Hepacivirus - genetics hepatitis C virus Methylation Mice Mice, Inbred C57BL Mice, Transgenic Microbiology Molecular Sequence Data Transgenes Virology |
| title | Inactivation of hepatitis C virus cDNA transgene by hypermethylation in transgenic mice |
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