Cytoplasmic inclusion cistron of Soybean mosaic virus serves as a virulence determinant on Rsv3 -genotype soybean and a symptom determinant
Abstract Soybean mosaic virus (SMV; Potyvirus , Potyviridae ) is one of the most widespread viruses of soybean globally. Three dominant resistance genes ( Rsv1 , Rsv3 and Rsv4 ) differentially confer resistance against SMV. Rsv1 confers extreme resistance and the resistance mechanism of Rsv4 is asso...
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Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 2009-09, Vol.391 (2), p.240-248 |
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description | Abstract Soybean mosaic virus (SMV; Potyvirus , Potyviridae ) is one of the most widespread viruses of soybean globally. Three dominant resistance genes ( Rsv1 , Rsv3 and Rsv4 ) differentially confer resistance against SMV. Rsv1 confers extreme resistance and the resistance mechanism of Rsv4 is associated with late susceptibility. Here, we show that Rsv3 restricts the accumulation of SMV strain G7 to the inoculated leaves, whereas, SMV-N, an isolate of SMV strain G2, establishes systemic infection. This observation suggests that the resistance mechanism of Rsv3 differs phenotypically from those of Rsv1 and Rsv4 . To identify virulence determinant(s) of SMV on an Rsv3 -genotype soybean, chimeras were constructed by exchanging fragments between avirulent SMV-G7 and the virulent SMV-N. Analyses of the chimeras showed that both the N- and C-terminal regions of the cytoplasmic inclusion (CI) cistron are required for Rsv3 -mediated resistance. Interestingly, the N-terminal region of CI is also involved in severe symptom induction in soybean. |
doi_str_mv | 10.1016/j.virol.2009.06.020 |
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Three dominant resistance genes ( Rsv1 , Rsv3 and Rsv4 ) differentially confer resistance against SMV. Rsv1 confers extreme resistance and the resistance mechanism of Rsv4 is associated with late susceptibility. Here, we show that Rsv3 restricts the accumulation of SMV strain G7 to the inoculated leaves, whereas, SMV-N, an isolate of SMV strain G2, establishes systemic infection. This observation suggests that the resistance mechanism of Rsv3 differs phenotypically from those of Rsv1 and Rsv4 . To identify virulence determinant(s) of SMV on an Rsv3 -genotype soybean, chimeras were constructed by exchanging fragments between avirulent SMV-G7 and the virulent SMV-N. Analyses of the chimeras showed that both the N- and C-terminal regions of the cytoplasmic inclusion (CI) cistron are required for Rsv3 -mediated resistance. Interestingly, the N-terminal region of CI is also involved in severe symptom induction in soybean.</description><identifier>ISSN: 0042-6822</identifier><identifier>EISSN: 1096-0341</identifier><identifier>DOI: 10.1016/j.virol.2009.06.020</identifier><identifier>PMID: 19595406</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>amino acid sequences ; Cytoplasmic inclusion ; cytoplasmic inclusion cistron ; disease resistance ; Genes ; Genotype ; Glycine max ; Glycine max - virology ; helper-component proteinase ; host-pathogen relationships ; hypersensitive response ; Inclusion Bodies ; Infectious Disease ; molecular sequence data ; pathogenesis ; Pathogenicity ; phenotypic variation ; Plant Diseases - virology ; plant viruses ; Potyviridae ; Potyvirus ; Potyvirus - genetics ; Potyvirus - pathogenicity ; Recombination, Genetic ; resistance mechanisms ; signs and symptoms (plants) ; site-directed mutagenesis ; Soybean mosaic virus ; soybeans ; Viral Proteins ; Virulence ; Virulence Factors</subject><ispartof>Virology (New York, N.Y.), 2009-09, Vol.391 (2), p.240-248</ispartof><rights>Elsevier Inc.</rights><rights>2009 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c578t-e663d6fd04fc1b353e0667de70623c4567c7fadd8df52fd46f3d7a264a3e54e33</citedby><cites>FETCH-LOGICAL-c578t-e663d6fd04fc1b353e0667de70623c4567c7fadd8df52fd46f3d7a264a3e54e33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.virol.2009.06.020$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19595406$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Chunquan</creatorcontrib><creatorcontrib>Hajimorad, M.R</creatorcontrib><creatorcontrib>Eggenberger, Alan L</creatorcontrib><creatorcontrib>Tsang, Stephanie</creatorcontrib><creatorcontrib>Whitham, Steven A</creatorcontrib><creatorcontrib>Hill, John H</creatorcontrib><title>Cytoplasmic inclusion cistron of Soybean mosaic virus serves as a virulence determinant on Rsv3 -genotype soybean and a symptom determinant</title><title>Virology (New York, N.Y.)</title><addtitle>Virology</addtitle><description>Abstract Soybean mosaic virus (SMV; Potyvirus , Potyviridae ) is one of the most widespread viruses of soybean globally. Three dominant resistance genes ( Rsv1 , Rsv3 and Rsv4 ) differentially confer resistance against SMV. Rsv1 confers extreme resistance and the resistance mechanism of Rsv4 is associated with late susceptibility. Here, we show that Rsv3 restricts the accumulation of SMV strain G7 to the inoculated leaves, whereas, SMV-N, an isolate of SMV strain G2, establishes systemic infection. This observation suggests that the resistance mechanism of Rsv3 differs phenotypically from those of Rsv1 and Rsv4 . To identify virulence determinant(s) of SMV on an Rsv3 -genotype soybean, chimeras were constructed by exchanging fragments between avirulent SMV-G7 and the virulent SMV-N. Analyses of the chimeras showed that both the N- and C-terminal regions of the cytoplasmic inclusion (CI) cistron are required for Rsv3 -mediated resistance. Interestingly, the N-terminal region of CI is also involved in severe symptom induction in soybean.</description><subject>amino acid sequences</subject><subject>Cytoplasmic inclusion</subject><subject>cytoplasmic inclusion cistron</subject><subject>disease resistance</subject><subject>Genes</subject><subject>Genotype</subject><subject>Glycine max</subject><subject>Glycine max - virology</subject><subject>helper-component proteinase</subject><subject>host-pathogen relationships</subject><subject>hypersensitive response</subject><subject>Inclusion Bodies</subject><subject>Infectious Disease</subject><subject>molecular sequence data</subject><subject>pathogenesis</subject><subject>Pathogenicity</subject><subject>phenotypic variation</subject><subject>Plant Diseases - virology</subject><subject>plant viruses</subject><subject>Potyviridae</subject><subject>Potyvirus</subject><subject>Potyvirus - genetics</subject><subject>Potyvirus - pathogenicity</subject><subject>Recombination, Genetic</subject><subject>resistance mechanisms</subject><subject>signs and symptoms (plants)</subject><subject>site-directed mutagenesis</subject><subject>Soybean mosaic virus</subject><subject>soybeans</subject><subject>Viral Proteins</subject><subject>Virulence</subject><subject>Virulence Factors</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkt-K1DAUxoso7rj6BIL2yrvWk6RN2wsFGfwHC4LjXodMcrpkbJMxpx3oM_jSpjsDijcLBw4Jv-8kfN_JspcMSgZMvj2UJxfDUHKArgRZAodH2YZBJwsQFXucbQAqXsiW86vsGdEB0rlp4Gl2xbq6qyuQm-z3dpnCcdA0OpM7b4aZXPC5cTTF1EOf78KyR-3zMZBOTHpzppwwnpByner-ZkBvMLc4YRyd137Kk_g7nURe3KEP03LEnC6DtLdJRct4nML4r-Z59qTXA-GLS7_Obj99_LH9Utx8-_x1--GmMHXTTgVKKazsLVS9YXtRCwQpG4sNSC5MVcvGNL22trV9zXtbyV7YRnNZaYF1hUJcZ2_Oc48x_JqRJjU6MjgM2mOYScmmbmvZyQdBnixvJecJFGfQxEAUsVfH6EYdF8VArWGpg7oPS61hKZAqKZPq1WX8vB_R_tVc0knA6zPQ66D0XXSkbnccmADWVjxVIt6dCUx-nRxGRcatWVgX0UzKBvfAF97_pzeD887o4ScuSIcwR5-iUEwRV6B260atCwUdQHK-Fn8ACZDH6Q</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>Zhang, Chunquan</creator><creator>Hajimorad, M.R</creator><creator>Eggenberger, Alan L</creator><creator>Tsang, Stephanie</creator><creator>Whitham, Steven A</creator><creator>Hill, John H</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>FBQ</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>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20090901</creationdate><title>Cytoplasmic inclusion cistron of Soybean mosaic virus serves as a virulence determinant on Rsv3 -genotype soybean and a symptom determinant</title><author>Zhang, Chunquan ; Hajimorad, M.R ; Eggenberger, Alan L ; Tsang, Stephanie ; Whitham, Steven A ; Hill, John H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c578t-e663d6fd04fc1b353e0667de70623c4567c7fadd8df52fd46f3d7a264a3e54e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>amino acid sequences</topic><topic>Cytoplasmic inclusion</topic><topic>cytoplasmic inclusion cistron</topic><topic>disease resistance</topic><topic>Genes</topic><topic>Genotype</topic><topic>Glycine max</topic><topic>Glycine max - virology</topic><topic>helper-component proteinase</topic><topic>host-pathogen relationships</topic><topic>hypersensitive response</topic><topic>Inclusion Bodies</topic><topic>Infectious Disease</topic><topic>molecular sequence data</topic><topic>pathogenesis</topic><topic>Pathogenicity</topic><topic>phenotypic variation</topic><topic>Plant Diseases - virology</topic><topic>plant viruses</topic><topic>Potyviridae</topic><topic>Potyvirus</topic><topic>Potyvirus - genetics</topic><topic>Potyvirus - pathogenicity</topic><topic>Recombination, Genetic</topic><topic>resistance mechanisms</topic><topic>signs and symptoms (plants)</topic><topic>site-directed mutagenesis</topic><topic>Soybean mosaic virus</topic><topic>soybeans</topic><topic>Viral Proteins</topic><topic>Virulence</topic><topic>Virulence Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Chunquan</creatorcontrib><creatorcontrib>Hajimorad, M.R</creatorcontrib><creatorcontrib>Eggenberger, Alan L</creatorcontrib><creatorcontrib>Tsang, Stephanie</creatorcontrib><creatorcontrib>Whitham, Steven A</creatorcontrib><creatorcontrib>Hill, John H</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Virology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Chunquan</au><au>Hajimorad, M.R</au><au>Eggenberger, Alan L</au><au>Tsang, Stephanie</au><au>Whitham, Steven A</au><au>Hill, John H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytoplasmic inclusion cistron of Soybean mosaic virus serves as a virulence determinant on Rsv3 -genotype soybean and a symptom determinant</atitle><jtitle>Virology (New York, N.Y.)</jtitle><addtitle>Virology</addtitle><date>2009-09-01</date><risdate>2009</risdate><volume>391</volume><issue>2</issue><spage>240</spage><epage>248</epage><pages>240-248</pages><issn>0042-6822</issn><eissn>1096-0341</eissn><abstract>Abstract Soybean mosaic virus (SMV; Potyvirus , Potyviridae ) is one of the most widespread viruses of soybean globally. Three dominant resistance genes ( Rsv1 , Rsv3 and Rsv4 ) differentially confer resistance against SMV. Rsv1 confers extreme resistance and the resistance mechanism of Rsv4 is associated with late susceptibility. Here, we show that Rsv3 restricts the accumulation of SMV strain G7 to the inoculated leaves, whereas, SMV-N, an isolate of SMV strain G2, establishes systemic infection. This observation suggests that the resistance mechanism of Rsv3 differs phenotypically from those of Rsv1 and Rsv4 . To identify virulence determinant(s) of SMV on an Rsv3 -genotype soybean, chimeras were constructed by exchanging fragments between avirulent SMV-G7 and the virulent SMV-N. Analyses of the chimeras showed that both the N- and C-terminal regions of the cytoplasmic inclusion (CI) cistron are required for Rsv3 -mediated resistance. Interestingly, the N-terminal region of CI is also involved in severe symptom induction in soybean.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19595406</pmid><doi>10.1016/j.virol.2009.06.020</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | amino acid sequences Cytoplasmic inclusion cytoplasmic inclusion cistron disease resistance Genes Genotype Glycine max Glycine max - virology helper-component proteinase host-pathogen relationships hypersensitive response Inclusion Bodies Infectious Disease molecular sequence data pathogenesis Pathogenicity phenotypic variation Plant Diseases - virology plant viruses Potyviridae Potyvirus Potyvirus - genetics Potyvirus - pathogenicity Recombination, Genetic resistance mechanisms signs and symptoms (plants) site-directed mutagenesis Soybean mosaic virus soybeans Viral Proteins Virulence Virulence Factors |
title | Cytoplasmic inclusion cistron of Soybean mosaic virus serves as a virulence determinant on Rsv3 -genotype soybean and a symptom determinant |
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