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dc.contributor.authorLee, Wing-Shamen
dc.contributor.authorFu, Shih-Fengen
dc.contributor.authorLi, Zhengen
dc.contributor.authorMurphy, Alexandraen
dc.contributor.authorDobson, Elizabeth Aen
dc.contributor.authorGarland, Lauraen
dc.contributor.authorChaluvadi, Srinivasa Raoen
dc.contributor.authorLewsey, Mathew Gen
dc.contributor.authorNelson, Richard Sen
dc.contributor.authorCarr, Johnen
dc.date.accessioned2016-01-07T14:09:26Z
dc.date.available2016-01-07T14:09:26Z
dc.date.issued2016-01-13en
dc.identifier.citationLee et al. BMC Plant Biology (2016), 16:15. doi: 10.1186/s12870-016-0705-8en
dc.identifier.issn1471-2229
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/253145
dc.description.abstractBackground: Host RNA-dependent RNA polymerases (RDRs) 1 and 6 contribute to antiviral RNA silencing in plants. RDR6 is constitutively expressed and was previously shown to limit invasion of Nicotiana benthamiana meristem tissue by potato virus X and thereby inhibit disease development. RDR1 is inducible by salicylic acid (SA) and several other phytohormones. But although it contributes to basal resistance to tobacco mosaic virus (TMV) it is dispensable for SA-induced resistance in inoculated leaves. The laboratory accession of N. benthamiana is a natural rdr1 mutant and highly susceptible to TMV. However, TMV-induced symptoms are ameliorated in transgenic plants expressing Medicago truncatula RDR1. Results: In MtRDR1-transgenic N. benthamiana plants the spread of TMV expressing the green fluorescent protein (TMV.GFP) into upper, non-inoculated, leaves was not inhibited. However, in these plants exclusion of TMV.GFP from the apical meristem and adjacent stem tissue was greater than in control plants and this exclusion effect was enhanced by SA. TMV normally kills N. benthamiana plants but although MtRDR1-transgenic plants initially displayed virus-induced necrosis they subsequently recovered. Recovery from disease was markedly enhanced by SA treatment in MtRDR1-transgenic plants whereas in control plants SA delayed but did not prevent systemic necrosis and death. Following SA treatment of MtRDR1-transgenic plants, extractable RDR enzyme activity was increased and Western blot analysis of RDR extracts revealed a band cross-reacting with an antibody raised against MtRDR1. Expression of MtRDR1 in the transgenic N. benthamiana plants was driven by a constitutive 35S promoter derived from cauliflower mosaic virus, confirmed to be non-responsive to SA. This suggests that the effects of SA on MtRDR1 are exerted at a post-transcriptional level. Conclusions: MtRDR1 inhibits severe symptom development by limiting spread of virus into the growing tips of infected plants. Thus, RDR1 may act in a similar fashion to RDR6. MtRDR1 and SA acted additively to further promote recovery from disease symptoms in MtRDR1-transgenic plants. Thus it is possible that SA promotes MtRDR1 activity and/or stability through post-transcriptional effects.
dc.description.sponsorshipWe thank Zhixiang Chen for his advice on the RDR assay protocol. Xiaoqiang Wang and Zhentian Lei at the Samuel Roberts Noble Foundation for the AKTA purification protocol and analysis of recombinant MBP:MtRDR1 fusion protein, respectively. David Baulcombe, Peter Palukaitis, Joel Milner and Lydia Hunter are thanked for stimulating discussions and useful advice and Adrienne Pate for expert technical assistance. FSF was funded by grants from the Cambridge Overseas Trust and the Ministry of Education of Taiwan, and WSL was funded by a studentship from the Biotechnology and Biological Sciences Research Council (BBSRC) and work in the Carr lab was funded by BBSRC grants (BB/D008204/1, BB/D014376/1, BB/J011762/1), The Leverhulme Trust (F/09 741/F, RPG-2012-667), and Cambridge University Isaac Newton Trust. RSN and SRC were funded by the Samuel Roberts Noble Foundation, Inc.
dc.languageEnglishen
dc.language.isoenen
dc.publisherBioMed Central
dc.rightsAttribution 2.0 UK: England & Wales
dc.rights.urihttp://creativecommons.org/licenses/by/2.0/uk/
dc.subjectsystemic acquired resistanceen
dc.subjecthypersensitive responseen
dc.subjectvirus movementen
dc.subjectRNAien
dc.subjectpost-transcriptional gene silencingen
dc.subjecteffector-triggered immunityen
dc.subjectdefensive signal transductionen
dc.titleSalicylic acid treatment and expression of an RNA-dependent RNA polymerase 1 transgene inhibit lethal symptoms and meristem invasion during tobacco mosaic virus infection in Nicotiana benthamianaen
dc.typeArticle
dc.description.versionThis is the final version of the article. It first appeared from BioMed Central via http://dx.doi.org/10.1186/s12870-016-0705-8en
prism.number15en
prism.publicationDate2016en
prism.publicationNameBMC Plant Biologyen
prism.volume16en
dc.rioxxterms.funderBBSRC
dc.rioxxterms.projectidBB/D008204/1
dc.rioxxterms.projectidBB/D014376/1
dc.rioxxterms.projectidBB/J011762/1
dcterms.dateAccepted2016-01-06en
rioxxterms.versionofrecord10.1186/s12870-016-0705-8en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2016-01-13en
dc.contributor.orcidMurphy, Alexandra [0000-0002-2226-8759]
dc.contributor.orcidCarr, John [0000-0002-5028-2160]
dc.identifier.eissn1471-2229
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idIsaac Newton Trust (1207(1))
pubs.funder-project-idBBSRC (BB/J011762/1)
pubs.funder-project-idBBSRC (BB/D008204/1)
pubs.funder-project-idBBSRC (BB/F014376/1)
cam.orpheus.successThu Jan 30 12:55:28 GMT 2020 - The item has an open VoR version.*
rioxxterms.freetoread.startdate2300-01-01


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Attribution 2.0 UK: England & Wales
Except where otherwise noted, this item's licence is described as Attribution 2.0 UK: England & Wales