Functional replacement of the tobacco rattle virus cysteine-rich protein by pathogenicity proteins from unrelated plant viruses.
Mutation of the 16K gene encoded by RNA1 of Tobacco rattle virus (TRV) greatly reduced the levels of viral RNA that accumulated in both infected protoplasts and plants, showing that the 16K cysteine-rich protein (CRP) is required for efficient multiplication of TRV. Overexpression of the 16K protein, either from an additional copy of the gene carried on TRV RNA2 or from a PVX vector, led to an increase in the severity of disease symptoms, suggesting that the protein has a role in the pathogenicity of the virus. Mutation of the 16K gene could be overcome by expression from RNA2 of the Cucumber mosaic virus 2b gene, the Soil-borne wheat mosaic virus 19K gene, or the Barley stripe mosaic virus gammab gene, indicating that the proteins encoded by these diverse genes may have similar functions. One known function of the CMV 2b gene is as a suppressor of posttranscriptional gene silencing, suggesting that the TRV 16K protein may also possess this activity.[1]References
- Functional replacement of the tobacco rattle virus cysteine-rich protein by pathogenicity proteins from unrelated plant viruses. Liu, H., Reavy, B., Swanson, M., MacFarlane, S.A. Virology (2002) [Pubmed]
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