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Plants respond to computer virus infections by activation of RNA-based silencing, which limits contamination at both the single-cell and system levels. RDR proteins. INTRODUCTION In plants and some animal lineages, such as insects, RNA silencing is usually a potent defense mechanism against viruses and has amazing specificity and adaptability (Ding 371935-79-4 supplier and Voinnet, 2007). To counter this defense mechanism, viruses encode suppressor proteins that interfere with RNA silencing. Antiviral silencing can be conceptualized into initiation, amplification, and systemic spread phases (Voinnet, 2005). Initiation consists of the recognition of the trigger RNA and formation of primary small interfering RNAs (siRNAs), while amplification is usually characterized by the synthesis of double-stranded RNA (dsRNA) by one or more RNA-dependent RNA polymerases and the formation of secondary siRNA. Systemic spread involves cell-to-cell and phloem-dependent transport of a silencing signal (Ding and Voinnet, 2007). Dicer-like ribonucleases (DCLs), Argonaute (AGO) proteins, dsRNA binding proteins (DRBs), and RNA-dependent RNA polymerase (RDR) proteins are core components of herb RNA silencing pathways involved in siRNA biogenesis or effector pathways. Four DCLs in catalyze formation of microRNAs (miRNAs; DCL1), or 22-nucleotide (DCL2), 24-nucleotide (DCL3), and 21-nucleotide (DCL4) siRNAs from several classes of dsRNA precursors. DCL1 functions with the dsRNA binding protein HYL1 and SERRATE to accurately process predominantly 21-nucleotide miRNAs from foldback precursors (Park et al., 2002; Reinhart et al., 2002; Han et al., 2004; Grigg et al., 2005; Dong et al., 2008). Most, but not all, miRNAs function in association with AGO1 (Vaucheret et al., 2004; Baumberger and Baulcombe, 2005; Qi et al., 2006; Mi et al., 2008). DCL4 functions with DRB4 to process RDR6-dependent dsRNA precursors for trans-acting siRNA (tasiRNA) (Gasciolli et al., 2005; Xie et al., 2005; Yoshikawa et al., 2005). Most tasiRNAs also function with AGO1 (Baumberger and Baulcombe, 2005; Mi et al., 2008). DCL3 functions to process RDR2-dependent dsRNA precursors that form at numerous endogenous loci, and at many of these loci, the resulting 24-nucleotide siRNAs function through AGO4/Pol V complexes to direct DRM2-dependent RNA-directed DNA methylation at cytosine positions in a CNN context (Cao and Jacobsen, 2002; Zilberman et al., 2003; Xie et al., 371935-79-4 supplier 2004; Li et al., 2006; Pontes et al., 2006; Wierzbicki et al., 2009). DCL2 is usually less well studied than the other DCL proteins, although it is known to play a role in formation of natural antisense siRNA and in transitive silencing of transgene transcripts (Borsani et al., Rabbit polyclonal to PCSK5 2005; Bouche et al., 2006; Mlotshwa et al., 2008). Antiviral RNA silencing depends on some of the core factors that participate in the biogenesis and activity of endogenous siRNAs (Ding and Voinnet, 2007). DCL4 catalyzes formation of 21-nucleotide siRNAs from several RNA and DNA viruses (Blevins et al., 2006; Deleris et al., 2006; Fusaro et al., 2006; Diaz-Pendon et al., 2007). In the absence of DCL4, 22- and 24-nucleotide-long virus-derived siRNAs are produced by DCL2 and DCL3, respectively (Blevins et al., 2006; Deleris et al., 2006; Fusaro et al., 2006; Diaz-Pendon et al., 2007). DCL1 may play an indirect role as a negative regulator of DCL4 (Qu et al., 2008) and as a facilitator in the biogenesis of geminivirus- and caulimovirus-derived siRNAs (Blevins et al., 2006; Moissiard and Voinnet, 2006). siRNA biogenesis or antiviral silencing have also been shown to be dependent on one or more of RDR1, RDR2, and RDR6 (Mourrain et al., 2000; Qu et al., 2005, 2008; Schwach et al., 2005; Diaz-Pendon et al., 2007; Donaire et al., 2008; Qi et al., 2009; Wang et al., 2010). Systemic RNA silencing in requires RDR1 and RDR6 for amplification of (CMV)-derived sRNAs (Wang et al., 2010). RDR1 may couple with other defense responses because its expression is usually induced by salicylic acid (Ji and Ding, 2001; Xie et al., 2001; Yu et al., 2003). It is noted, however, that most studies to date do not clearly link virus-derived siRNA accumulation patterns 371935-79-4 supplier and bona fide antiviral defense where the computer virus is actually suppressed or limited. When wild-type viruses are used, the activity of a virus-encoded silencing suppressor can mask the activity of silencing factors. Thus, wild-type plants often exhibit computer virus susceptibility phenotypes similar to those of mutants that lack RNA silencing factors (Dalmay.