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Divergence of host range and biological properties between natural isolate and full‐length infectious cDNA clone of the B eet mild yellowing virus   2ITB
Author(s) -
Klein Elodie,
Brault Véronique,
Klein Delphine,
Weyens Guy,
Lefèbvre Marc,
ZieglerGraff Véronique,
Gilmer David
Publication year - 2014
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12061
Subject(s) - biology , virology , nicotiana benthamiana , virus , infectivity , complementary dna , cucumovirus , potato virus x , clone (java method) , plant virus , cucumber mosaic virus , gene , genetics
Summary Plant infection by poleroviruses is restricted to phloem tissues, preventing any classical leaf rub inoculation with viral RNA or virions. Efficient virus inoculation to plants is achieved by viruliferous aphids that acquire the virus by feeding on infected plants. The use of promoter‐driven infectious cDNA is an alternative means to infect plants and allows reverse genetic studies to be performed. Using B eet mild yellowing virus isolate 2ITB ( BMYV ‐ 2ITB ), we produced a full‐length infectious cDNA clone of the virus (named BMYV‐EK ) placed under the control of the T7 RNA polymerase and the C auliflower mosaic virus   35S promoters. Infectivity of the engineered BMYV‐EK virus was assayed in different plant species and compared with that of the original virus. We showed that in vitro ‐ or in planta ‐derived transcripts were infectious in protoplasts and in whole plants. Importantly, the natural aphid vector M yzus persicae efficiently transmitted the viral progeny produced in infected plants. By comparing agroinoculation and aphid infection in a host range assay, we showed that the engineered BMYV‐EK virus displayed a similar host range to BMYV‐2ITB , except for N icotiana benthamiana , which proved to be resistant to systemic infection with BMYV‐EK . Finally, both the BMYV‐EK P0 and the full‐length clone were able to strongly interfere with post‐transcriptional gene silencing.

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