An Antiviral Role for the RNA Interference Machinery in Caenorhabditis elegans
RNA interference (RNAi) is a sequence-specific gene-silencing mechanism triggered by exogenous dsRNA. In plants an RNAi-like mechanism defends against viruses, but the hypothesis that animals possess a similar natural antiviral mechanism related to RNAi remains relatively untested. To test whether g...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2005-12, Vol.102 (51), p.18420-18424 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Schott, Daniel H. David K. Cureton Whelan, Sean P. Hunter, Craig P. Sharp, Phillip A. |
| description | RNA interference (RNAi) is a sequence-specific gene-silencing mechanism triggered by exogenous dsRNA. In plants an RNAi-like mechanism defends against viruses, but the hypothesis that animals possess a similar natural antiviral mechanism related to RNAi remains relatively untested. To test whether genes needed for RNAi defend animal cells against virus infection, we infected wild-type and RNAi-defective cells of the nematode C. elegans with vesicular stomatitis virus engineered to encode a GFP fusion protein. We show that upon infection, cells lacking components of the RNAi apparatus produce more GFP and infective particles than wild-type cells. Furthermore, we show that mutant cells with enhanced RNAi produce less GFP. Our observation that multiple genes required for RNAi are also required for resistance to vesicular stomatitis virus suggests that the RNAi machinery functions in resistance to viruses in nature. |
| doi_str_mv | 10.1073/pnas.0507123102 |
| format | Article |
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Cureton ; Whelan, Sean P. ; Hunter, Craig P. ; Sharp, Phillip A.</creator><creatorcontrib>Schott, Daniel H. ; David K. Cureton ; Whelan, Sean P. ; Hunter, Craig P. ; Sharp, Phillip A.</creatorcontrib><description>RNA interference (RNAi) is a sequence-specific gene-silencing mechanism triggered by exogenous dsRNA. In plants an RNAi-like mechanism defends against viruses, but the hypothesis that animals possess a similar natural antiviral mechanism related to RNAi remains relatively untested. To test whether genes needed for RNAi defend animal cells against virus infection, we infected wild-type and RNAi-defective cells of the nematode C. elegans with vesicular stomatitis virus engineered to encode a GFP fusion protein. We show that upon infection, cells lacking components of the RNAi apparatus produce more GFP and infective particles than wild-type cells. Furthermore, we show that mutant cells with enhanced RNAi produce less GFP. 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Cureton</creatorcontrib><creatorcontrib>Whelan, Sean P.</creatorcontrib><creatorcontrib>Hunter, Craig P.</creatorcontrib><creatorcontrib>Sharp, Phillip A.</creatorcontrib><title>An Antiviral Role for the RNA Interference Machinery in Caenorhabditis elegans</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>RNA interference (RNAi) is a sequence-specific gene-silencing mechanism triggered by exogenous dsRNA. In plants an RNAi-like mechanism defends against viruses, but the hypothesis that animals possess a similar natural antiviral mechanism related to RNAi remains relatively untested. To test whether genes needed for RNAi defend animal cells against virus infection, we infected wild-type and RNAi-defective cells of the nematode C. elegans with vesicular stomatitis virus engineered to encode a GFP fusion protein. We show that upon infection, cells lacking components of the RNAi apparatus produce more GFP and infective particles than wild-type cells. Furthermore, we show that mutant cells with enhanced RNAi produce less GFP. Our observation that multiple genes required for RNAi are also required for resistance to vesicular stomatitis virus suggests that the RNAi machinery functions in resistance to viruses in nature.</description><subject>Animal cells</subject><subject>Animals</subject><subject>Biological Sciences</subject><subject>Biophysics</subject><subject>Botany</subject><subject>Caenorhabditis elegans</subject><subject>Caenorhabditis elegans - genetics</subject><subject>Caenorhabditis elegans - immunology</subject><subject>Caenorhabditis elegans - virology</subject><subject>Cell culture techniques</subject><subject>Cells</subject><subject>Cells, Cultured</subject><subject>Double stranded RNA</subject><subject>Embryonic cells</subject><subject>Fluorescence</subject><subject>Genes, Reporter - genetics</subject><subject>Infections</subject><subject>Kidney cells</subject><subject>Mutation - genetics</subject><subject>Nematoda</subject><subject>Rhabdoviridae Infections - immunology</subject><subject>Rhabdoviridae Infections - virology</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA Interference - physiology</subject><subject>Vesicular stomatitis Indiana virus - immunology</subject><subject>Vesicular stomatitis Indiana virus - physiology</subject><subject>Vesicular stomatitis virus</subject><subject>Viruses</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c9v0zAUB3ALgVgpnLkgZHFA4pDtPdtJ7AtSVfFj0hjSBGfLSV7WVKldbHdi_z2pWq3AZScf_HlfPfvL2GuEc4RaXmy9S-dQQo1CIognbIZgsKiUgadsBiDqQiuhztiLlNYAYEoNz9kZVlIaAzhj1wvPFz4Pd0N0I78JI_E-RJ5XxG-uF_zSZ4o9RfIt8W-uXQ2e4j0fPF868iGuXNMNeUicRrp1Pr1kz3o3Jnp1POfs5-dPP5Zfi6vvXy6Xi6uiLYXJhVSN6g1oEACldI1uFVKFUitNCruejG6NMoI6JRqpja5JmB661qBs0LVyzj4ecre7ZkNdSz5P-9ttHDYu3tvgBvvvjR9W9jbcWZRYGymngPfHgBh-7ShluxlSS-PoPIVdspU2qCv9OESj0VTTK-bs3X9wHXbRT79gBaCsVFnv0y4OqI0hpUj9w8oIdt-o3TdqT41OE2__funJHyucAD-C_eQpTtgSLU7tw0Q-PEJsvxvHTL_zZN8c7DrlEB-wwlJUUsg_4uK9Ug</recordid><startdate>20051220</startdate><enddate>20051220</enddate><creator>Schott, Daniel H.</creator><creator>David K. 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Cureton ; Whelan, Sean P. ; Hunter, Craig P. ; Sharp, Phillip A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c529t-34b4f908020053ab8c41e613848e41dfe98c9492ed42b38987e29f0dc913b1ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animal cells</topic><topic>Animals</topic><topic>Biological Sciences</topic><topic>Biophysics</topic><topic>Botany</topic><topic>Caenorhabditis elegans</topic><topic>Caenorhabditis elegans - genetics</topic><topic>Caenorhabditis elegans - immunology</topic><topic>Caenorhabditis elegans - virology</topic><topic>Cell culture techniques</topic><topic>Cells</topic><topic>Cells, Cultured</topic><topic>Double stranded RNA</topic><topic>Embryonic cells</topic><topic>Fluorescence</topic><topic>Genes, Reporter - genetics</topic><topic>Infections</topic><topic>Kidney cells</topic><topic>Mutation - genetics</topic><topic>Nematoda</topic><topic>Rhabdoviridae Infections - immunology</topic><topic>Rhabdoviridae Infections - virology</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA Interference - physiology</topic><topic>Vesicular stomatitis Indiana virus - immunology</topic><topic>Vesicular stomatitis Indiana virus - physiology</topic><topic>Vesicular stomatitis virus</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schott, Daniel H.</creatorcontrib><creatorcontrib>David K. 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| subjects | Animal cells Animals Biological Sciences Biophysics Botany Caenorhabditis elegans Caenorhabditis elegans - genetics Caenorhabditis elegans - immunology Caenorhabditis elegans - virology Cell culture techniques Cells Cells, Cultured Double stranded RNA Embryonic cells Fluorescence Genes, Reporter - genetics Infections Kidney cells Mutation - genetics Nematoda Rhabdoviridae Infections - immunology Rhabdoviridae Infections - virology Ribonucleic acid RNA RNA Interference - physiology Vesicular stomatitis Indiana virus - immunology Vesicular stomatitis Indiana virus - physiology Vesicular stomatitis virus Viruses |
| title | An Antiviral Role for the RNA Interference Machinery in Caenorhabditis elegans |
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