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Journal of Virology, November 2007, p. 11768-11780, Vol. 81, No. 21
0022-538X/07/$08.00+0     doi:10.1128/JVI.01230-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The p122 Subunit of Tobacco Mosaic Virus Replicase Is a Potent Silencing Suppressor and Compromises both Small Interfering RNA- and MicroRNA-Mediated Pathways{triangledown}

Tibor Csorba,1,2 Aurelie Bovi,3 Tamás Dalmay,3* and József Burgyán1*

Agricultural Biotechnology Center, Plant Biology Institute, P.O. Box 411, H-2101 Gödöllo, Hungary,1 Department of Genetics, Eötvös Lóránd University, Budapest, Hungary,2 University of East Anglia, Norwich, United Kingdom3

Received 5 June 2007/ Accepted 10 August 2007

One of the functions of RNA silencing in plants is to defend against molecular parasites, such as viruses, retrotransposons, and transgenes. Plant viruses are inducers, as well as targets, of RNA silencing-based antiviral defense. Replication intermediates or folded viral RNAs activate RNA silencing, generating small interfering RNAs (siRNAs), which are the key players in the antiviral response. Viruses are able to counteract RNA silencing by expressing silencing-suppressor proteins. It has been shown that many of the identified silencing-suppressor proteins bind long double-stranded RNA or siRNAs and thereby prevent assembly of the silencing effector complexes. In this study, we show that the 122-kDa replicase subunit (p122) of crucifer-infecting Tobacco mosaic virus (cr-TMV) is a potent silencing-suppressor protein. We found that the p122 protein preferentially binds to double-stranded 21-nucleotide (nt) siRNA and microRNA (miRNA) intermediates with 2-nt 3' overhangs inhibiting the incorporation of siRNA and miRNA into silencing-related complexes (e.g., RNA-induced silencing complex [RISC]) both in vitro and in planta but cannot interfere with previously programmed RISCs. In addition, our results also suggest that the virus infection and/or sequestration of the siRNA and miRNA molecules by p122 enhances miRNA accumulation despite preventing its methylation. However, the p122 silencing suppressor does not prevent the methylation of certain miRNAs in hst-15 mutants, in which the nuclear export of miRNAs is compromised.

* Corresponding author. Mailing address for J. Burgyán: P. O. Box 411, H-2101 Gödöllo, Hungary. Phone: 36-28-526-155. Fax: 36-28-526-145. E-mail: burgyan{at}abc.hu. Mailing address for T. Dalmay: University of East Anglia, Norwich, United Kingdom. Phone: 44 1603 593221. Fax: 44 1603 592250. E-mail: T.Dalmay{at}uea.ac.uk

{triangledown} Published ahead of print on 22 August 2007.

Journal of Virology, November 2007, p. 11768-11780, Vol. 81, No. 21
0022-538X/07/$08.00+0     doi:10.1128/JVI.01230-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Martinez-Turino, S., Hernandez, C. (2009). Inhibition of RNA silencing by the coat protein of Pelargonium flower break virus: distinctions from closely related suppressors. J. Gen. Virol. 90: 519-525 [Abstract] [Full Text]  
  • Lozsa, R., Csorba, T., Lakatos, L., Burgyan, J. (2008). Inhibition of 3' modification of small RNAs in virus-infected plants require spatial and temporal co-expression of small RNAs and viral silencing-suppressor proteins. Nucleic Acids Res 36: 4099-4107 [Abstract] [Full Text]  


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