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First published online January 7, 2009; 10.1104/pp.108.132688 Plant Physiology 149:1399-1407 (2009) © 2009 American Society of Plant Biologists
Compromised Virus-Induced Gene Silencing in RDR6-Deficient Plants1,[W]Centre for Novel Agricultural Products (F.E.V.) and Department of Biology (F.E.V., L.J.), University of York, York YO10 5DD, United Kingdom
RNA silencing in plants serves as a potent antiviral defense mechanism through the action of small interfering RNAs (siRNAs), which direct RNA degradation. siRNAs can be derived directly from the viral genome or via the action of host-encoded RNA-dependent RNA polymerases (RDRs). Plant genomes encode multiple RDRs, and it has been demonstrated that plants defective for RDR6 hyperaccumulate several classes of virus. In this study, we compared the effectiveness of virus-induced gene silencing (VIGS) and RNA-directed DNA methylation (RdDM) in wild-type and RDR6-deficient Nicotiana benthamiana plants. For the potexvirus Potato virus X (PVX) and the potyvirus Plum pox virus (PPV), the efficiency of both VIGS and RdDM were compromised in RDR6-defective plants despite accumulating high levels of viral siRNAs similar to infection of wild-type plants. The reduced efficiency of VIGS and RdDM was unrelated to the size class of siRNA produced and, at least for PVX, was not dependent on the presence of the virus-encoded silencing suppressor protein, 25K. We suggest that primary siRNAs produced from PVX and PPV in the absence of RDR6 may not be good effectors of silencing and that RDR6 is required to produce secondary siRNAs that drive a more effective antiviral response.
1 This work was supported by the Garfield Weston Foundation. The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Fabián E. Vaistij (fv4{at}york.ac.uk). [W] The online version of this article contains Web-only data. www.plantphysiol.org/cgi/doi/10.1104/pp.108.132688 * Corresponding author; e-mail fv4{at}york.ac.uk. Received November 16, 2008; accepted December 31, 2008; published January 7, 2009.
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