Nucleic Acids Research Advance Access published online on September 18, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn590
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Gene regulation, Chromatin and Epigenetics |
The CaMV transactivator/viroplasmin interferes with RDR6-dependent trans-acting and secondary siRNA pathways in Arabidopsis
1Institute of Botany, University of Basel, Schönbeinstrasse 6, 4056 Basel, 2Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058 Basel, Switzerland and 3Division of Plant Sciences, 108 Waters Hall, University of Missouri, Columbia, MO 65211, USA
*To whom correspondence should be addressed. Tel: +4161 2672977; Fax: +4161 2673504; Email: Mikhail.Pooggin{at}unibas.ch
Received August 1, 2008. Revised August 29, 2008. Accepted September 2, 2008.
Several RNA silencing pathways in plants restrict viral infections and are suppressed by distinct viral proteins. Here we show that the endogenous trans-acting (ta)siRNA pathway, which depends on Dicer-like (DCL) 4 and RNA-dependent RNA polymerase (RDR) 6, is suppressed by infection of Arabidopsis with Cauliflower mosaic virus (CaMV). This effect was associated with overaccumulation of unprocessed, RDR6-dependent precursors of tasiRNAs and is due solely to expression of the CaMV transactivator/viroplasmin (TAV) protein. TAV expression also impaired secondary, but not primary, siRNA production from a silenced transgene and increased accumulation of mRNAs normally silenced by the four known tasiRNA families and RDR6-dependent secondary siRNAs. Moreover, TAV expression upregulated DCL4, DRB4 and AGO7 that mediate tasiRNA biogenesis. Our findings suggest that TAV is a general inhibitor of silencing amplification that impairs DCL4-mediated processing of RDR6-dependent double-stranded RNA to siRNAs. The resulting deficiency in tasiRNAs and other RDR6-/DCL4-dependent siRNAs appears to trigger a feedback mechanism that compensates for the inhibitory effects.
Present addresses: Padubidri V. Shivaprasad, Department of Plant Sciences, University of Cambridge, Cambridge CB2 3EA, UK
Todd Blevins, Biology Department, Washington University, St Louis, MO, USA
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