PLANT VIRAL SYNERGISM - THE POTYVIRAL GENOME ENCODES A BROAD-RANGE PATHOGENICITY ENHANCER THAT TRANSACTIVATES REPLICATION OF HETEROLOGOUS VIRUSES

Citation
G. Pruss et al., PLANT VIRAL SYNERGISM - THE POTYVIRAL GENOME ENCODES A BROAD-RANGE PATHOGENICITY ENHANCER THAT TRANSACTIVATES REPLICATION OF HETEROLOGOUS VIRUSES, The Plant cell, 9(6), 1997, pp. 859-868
Citations number
44
Categorie Soggetti
Biology,"Plant Sciences
Journal title
ISSN journal
10404651
Volume
9
Issue
6
Year of publication
1997
Pages
859 - 868
Database
ISI
SICI code
1040-4651(1997)9:6<859:PVS-TP>2.0.ZU;2-F
Abstract
Synergistic viral diseases of higher plants are caused by the interact ion of two independent viruses in the same host and are characterized by dramatic increases in symptoms and in accumulation of one of the co infecting viruses. In potato virus X (PVX/potyviral synergism, increas ed pathogenicity and accumulation of PVX are mediated by the expressio n of potyviral 5' proximal sequences encoding P1, the helper component proteinase (HC-Pro), and a fraction of P3. Here, we report that the s ame potyviral sequence (termed P1/HC-Pro) enhances the pathogenicity a nd accumulation of two other heterologous viruses: cucumber mosaic vir us and tobacco mosaic virus. In the case of PVX-potyviral synergism, w e show that the expression of the HC-Pro gene product, but not the RNA sequence itself, is sufficient to induce the increase in PVX pathogen icity and that both P1 and P3 coding sequences are dispensable for thi s aspect of the synergistic interaction. In protoplasts, expression of the potyviral P1/HC-Pro region prolongs the accumulation of PVX (-) s trand RNA and transactivates expression of a reporter gene from a PVX subgenomic promoter. Unlike the synergistic enhancement of PVX pathoge nicity, which requires only expression of HC-Pro, the enhancement of P VX (-) strand RNA accumulation in protoplasts is significantly greater when the entire P1/HC-Pro sequence is expressed. These results indica te that the potyviral P1/HC-Pro region affects a step in disease devel opment that is common to a broad range of virus infections and suggest a mechanism involving transactivation of viral replication.