Plant Physiol. Journal of Pharmacology and Experimental Therapeutics
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First published online July 3, 2008; 10.1104/pp.108.120808

Plant Physiology 148:414-423 (2008)
© 2008 American Society of Plant Biologists

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PLANTS INTERACTING WITH OTHER ORGANISMS

Viroid-Induced Symptoms in Nicotiana benthamiana Plants Are Dependent on RDR6 Activity1,[C],[W]

Gustavo Gómez, Germán Martínez and Vicente Pallás*

Instituto de Biología Molecular y Celular de Plantas, Consejo Superior de Investigaciones Científicas-Universidad Politécnica de Valencia, 46022 Valencia, Spain

Viroids are small self-replicating RNAs that infect plants. How these noncoding pathogenic RNAs interact with hosts to induce disease symptoms is a long-standing unanswered question. Recent experimental data have led to the suggestive proposal of a pathogenic model based on the RNA silencing mechanism. However, evidence of a direct relation between key components of the RNA silencing pathway and symptom expression in infected plants remains elusive. To address this issue, we used a symptomatic transgenic line of Nicotiana benthamiana that expresses and processes dimeric forms of Hop stunt viroid (HSVd). These plants were analyzed under different growing temperature conditions and were used as stocks in grafting assays with the rdr6i-Nb line, in which the RNA-dependent RNA polymerase 6 (RDR6) is constitutively silenced. Here, we show that the symptom expression in N. benthamiana plants is independent of HSVd accumulation levels but dependent on an active state of the viroid-specific RNA silencing pathway. The scion of rdr6i-Nb plants remained asymptomatic when grafted onto symptomatic plants, despite an accumulation of a high level of mature forms of HSVd, indicating the requirement of RDR6 for viroid-induced symptom production. In addition, the RDR6 requirement for symptom expression was also observed in wild-type N. benthamiana plants mechanically infected with HSVd. These results provide biological evidence of the involvement of the viroid-specific RNA silencing pathway in the symptom expression associated with viroid pathogenesis.


1 This work was supported by the Spanish granting agency Dirección General de Investigacion Cientifica y Technica (grant no. BIO2005–07331) and by the Generalitat Valenciana (grant no. GV05–238). G.G. is the recipient of a contract from the Consejo Superior de Investigaciones Científicas. G.M. is the recipient of a fellowship from the Ministry of Education and Science.

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: Vicente Pallás (vpallas{at}ibmcp.upv.es).

[C] Some figures in this article are displayed in color online but in black and white in the print edition.

[W] The online version of this article contains Web-only data.

www.plantphysiol.org/cgi/doi/10.1104/pp.108.120808

* Corresponding author; e-mail vpallas{at}ibmcp.upv.es.

Received April 11, 2008; accepted June 29, 2008; published July 3, 2008.


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