Skip to main content
ARS Home » Northeast Area » Frederick, Maryland » Foreign Disease-Weed Science Research » Research » Publications at this Location » Publication #205821

Title: Synthesis of minus-strand copies of a viral transgene during viral infections of transgenic plants

Author
item DENG, MIN - MICHIGAN STATE UNIVERSITY
item Schneider, William
item ALLISON, RICHARD - MICHIGAN STATE UNIVERSITY

Submitted to: Virus Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/31/2006
Publication Date: 5/31/2006
Citation: Deng, M., Schneider, W.L., Allison, R. 2006. Synthesis of minus-strand copies of a viral transgene during viral infections of transgenic plants. Virus Research.10.1016/ 2006.05.009.

Interpretive Summary: One of the common concerns about genetically modified organisms (GMOs), particularly virus resistant genetically modified crops, is that the expressed gene from a virus source could act as a source of new genetic information. In theory, this could have the effect of increasing the rate of viral evolution in GMO crops via recombination, in a similar manner to the evolution of new influenza virus strains. This paper desribes work that demonstrates that the viral gene products expressed by a transgenic plant are available to infecting viruses as a replication template, which is significant because this is how RNA-RNA recombination is thought to occur during replication. However, the paper also demonstrates that the level of viral replication of transgene RNA is extremely low, indicating that the likelihood of a recombination event leading to the evolution of new strains is virtually negligible. In fact, the likelihood of recombination in GMO crops is very likely much less than the likelihood of recombination and evolution in naturally occurring mixed infections of multiple viruses.

Technical Abstract: Plants can be genetically engineered to express viral sequences, often resulting in resistance to the virus from which the sequence was derived. The generally accepted mechanism for this pathogen induced resistance is gene silencing. Previous work has demonstrated that viral transgenes can be incorporated into viral RNAs via recombination. This is considered significant because recombination between viral RNAs is thought to be one of the mechanisms by which plant RNA viruses evolve. This paper demonstrates that viral replicases from invading viruses are capable of recognizing viral transgene RNA as a template, which is significant because RNA-RNA recombination in RNA viruses is thought to occur by a template switching mechanism. In addition this paper demonstrates that viral replicases from related viruses are capable of recognizing viral transgenes as templates, potentially leading to chimeric viruses. However, the levels of RNA produced from the viral transgene are remarkably low, detectable only occasionally by PCR, suggesting that these risks are rather minimal compared to the chances of RNA-RNA recombination occurring in natural mixed infections.