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Title: Phloem limitation of potato leafroll virus is an asset not a liability

Author
item PETER, KARI - CORNELL UNIVERSITY
item PALUKAITIS, PETER - SCOTTISH CROP RES INST
item BUSSAN, A. - UNIVERSITY OF WISCONSIN
item Gray, Stewart

Submitted to: Phytopathology
Publication Type: Abstract Only
Publication Acceptance Date: 3/1/2008
Publication Date: 7/1/2008
Citation: Peter, K., Palukaitis, P., Bussan, A., Gray, S.M. 2008. Phloem limitation of potato leafroll virus is an asset not a liability. Phytopathology. 98:S124.

Interpretive Summary:

Technical Abstract: Unlike most plant viruses, those that are grouped in the family Luteoviridae are restricted to phloem tissues and are considered to lack required movement proteins or plant anti-defense mechanisms that would allow them access to other host tissues. We report that potato leafroll virus (PLRV) actually selects for a protein-mediated mechanism that limits virus to the phloem. PLRV and related viruses encode an extension of their major capsid protein translated inefficiently via a readthrough mechanism. This multifunctional readthrough domain when incorporated into the virion is required for aphid transmission. The readthrough protein also functions in trans as a movement protein by facilitating long distance movement and accumulation of virus in phloem tissue. Mutations that eliminate translation of the C-terminal half of the readthrough domain reduce the rate of virus movement in phloem and the number of infection foci. Unexpectedly, virus that is unable to translate either the entire readthrough domain or the C-terminal half of the domain was mechanically transmissible to Solanum sarrachoides (Hairy Nightshade), and in both inoculated and systemically infected tissue, the virus was able to escape its phloem limitation and infect mesophyll cells. Crystalline arrays of virions were observed associated with chloroplast membranes in mesophyll cells. Wild type virus was not mechanically transmissible and was observed only in phloem associated cells. However, the ability of the mutant viruses to move into mesophyll cells was short lived. Compensatory mutations were positively selected that restored translation of the entire readthrough domain and re-established the phloem-specific distribution of the virus. Phloem limitation of the luteoviridae is not a deficiency, but may have evolved to facilitate transmission and ensure continued dispersal to new hosts. A model for virus movement encompassing these observations will be presented.