Publication | Open Access
Plant viral synergism: the potyviral genome encodes a broad-range pathogenicity enhancer that transactivates replication of heterologous viruses.
588
Citations
39
References
1997
Year
Heterologous VirusesViral ReplicationGeneticsViral Polymerase MechanismMolecular BiologyReporter GenePlant PathologyPlant VirologyPotato Virus XPlant Viral SynergismMosaic VirusPlant-virus InteractionPotyviral GenomeVirus GeneViral GeneticsPlant VirusVirologyGene ExpressionMolecular VirologyNatural SciencesPathogenesisMicrobiologyMedicine
Synergistic viral diseases in higher plants arise when two independent viruses co‑infect a host, producing markedly enhanced symptoms and accumulation of one virus, as seen in PVX–potyvirus interactions mediated by potyviral 5′ proximal sequences encoding P1, HC‑Pro, and part of P3. The study demonstrates that the potyviral P1/HC‑Pro sequence also boosts pathogenicity and accumulation of the heterologous viruses cucumber mosaic virus and tobacco mosaic virus. Expression of the potyviral HC‑Pro protein alone increases PVX pathogenicity, while the full P1/HC‑Pro region prolongs PVX (-) strand RNA accumulation and activates a subgenomic promoter, indicating that this region broadly enhances viral replication through transactivation.
Synergistic viral diseases of higher plants are caused by the interaction of two independent viruses in the same host and are characterized by dramatic increases in symptoms and in accumulation of one of the coinfecting viruses. In potato virus X (PVX)/potyviral synergism, increased pathogenicity and accumulation of PVX are mediated by the expression of potyviral 5' proximal sequences encoding P1, the helper component proteinase (HC-Pro), and a fraction of P3. Here, we report that the same potyviral sequence (termed P1/HC-Pro) enhances the pathogenicity and accumulation of two other heterologous viruses: cucumber mosaic virus and tobacco mosaic virus. In the case of PVX-potyviral synergism, we show that the expression of the HC-Pro gene product, but not the RNA sequence itself, is sufficient to induce the increase in PVX pathogenicity and that both P1 and P3 coding sequences are dispensable for this aspect of the synergistic interaction. In protoplasts, expression of the potyviral P1/HC-Pro region prolongs the accumulation of PVX (-) strand RNA and transactivates expression of a reporter gene from a PVX subgenomic promoter. Unlike the synergistic enhancement of PVX pathogenicity, which requires only expression of HC-Pro, the enhancement of PVX (-) strand RNA accumulation in protoplasts is significantly greater when the entire P1/HC-Pro sequence is expressed. These results indicate that the potyviral P1/HC-Pro region affects a step in disease development that is common to a broad range of virus infections and suggest a mechanism involving transactivation of viral replication.
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