Article

Direct and Indirect Roles of Viral Suppressors of RNA Silencing in Pathogenesis

Center for Plant Cell Biology, Department of Plant Pathology and Microbiology, University of California, Riverside, California 92521, USA.
Annual Review of Phytopathology (Impact Factor: 9.62). 10/2008; 46(1):303-26. DOI: 10.1146/annurev.phyto.46.081407.104746
Source: PubMed

ABSTRACT

Plant and animal viruses overcome host antiviral silencing by encoding diverse viral suppressors of RNA silencing (VSRs). Prior to the identification and characterization of their silencing suppression activities mostly in transgene silencing assays, plant VSRs were known to enhance virus accumulation in the inoculated protoplasts, promote cell-to-cell virus movement in the inoculated leaves, facilitate the phloem-dependent long-distance virus spread, and/or intensify disease symptoms in systemically infected tissues. Here we discuss how the various silencing suppression activities of VSRs may facilitate these distinct steps during plant infection and why VSRs may not play a direct role in eliciting disease symptoms by general impairments of host endogenous small RNA pathways. We also highlight many of the key questions still to be addressed on the role of viral suppression of antiviral silencing in plant infection.

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    • "and Arabidopsis thaliana (Díaz-Pendón and Ding, 2008). However, transgenic expression of RSS in non-natural hosts does not necessarily reflect the effects of viral infection, because, in their natural context, these proteins are often expressed only in infected cells and tissues, unlike the constitutively expressed transgenes (Csorba et al., 2009; Díaz-Pendón and Ding, 2008). Alternatively, mutant viruses expressing dysfunctional proteins have been used to assess their role as pathogenicity determinants (Hsieh et al., 2009; Yambao et al., 2008; Ziebell and Carr, 2009). "

    No preview · Article · Jan 2015 · Acta horticulturae
    • "and Arabidopsis thaliana (Díaz-Pendón and Ding, 2008). However, transgenic expression of RSS in non-natural hosts does not necessarily reflect the effects of viral infection, because, in their natural context, these proteins are often expressed only in infected cells and tissues, unlike the constitutively expressed transgenes (Csorba et al., 2009; Díaz-Pendón and Ding, 2008). Alternatively, mutant viruses expressing dysfunctional proteins have been used to assess their role as pathogenicity determinants (Hsieh et al., 2009; Yambao et al., 2008; Ziebell and Carr, 2009). "
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    ABSTRACT: Citrus tristeza virus (CTV) is phloem-restricted in natural citrus hosts. The 23 kDa protein (p23) encoded by the virus is an RNA silencing suppressor and a pathogenicity determinant. Expression of p23, or its N-terminal 157 amino acid fragment comprising the zinc-finger and flanking basic motifs, driven by the constitutive 35S promoter of cauliflower mosaic virus incites CTV-like symptoms and other aberrations in transgenic citrus. To better define the role of p23 in CTV pathogenesis, we compared the phenotypes of Mexican limes transformed with p23-derived transgenes from the severe T36 or the mild T317 CTV isolates under the control of the phloem-specific promoter from commelina yellow mottle virus (CoYMV) or the 35S promoter. Expression of the constructs restricted to the phloem incited a phenotype resembling CTV-specific symptoms (vein clearing and necrosis, and stem pitting), but not the non-specific aberrations (like mature leaf epinasty and yellow pinpoints, growth cease and apical necrosis) observed when p23 was ectopically expressed. Furthermore, vein necrosis and stem pitting in Mexican lime appeared specifically associated with p23 from T36. Phloem-specific accumulation of the p23Δ158-209(T36) fragment was sufficient to incite the same anomalies, indicating that the region comprising the N-terminal 157 amino acids of p23 is responsible (at least in part) for the vein clearing, stem pitting and possibly vein corking in this host.
    No preview · Article · Aug 2014 · Molecular Plant Pathology
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    • "To counter this antiviral defense, most plant viruses identified to date encode viral suppressors of RNA silencing (VSRs), which inhibit or inactivate various components of the RNA-silencing pathways (3, 4). Additionally, many VSR molecules play important roles in viral symptom induction (5). "
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    ABSTRACT: Unlabelled: The Cucumber Mosaic Virus (CMV) 2b protein is an RNA-silencing suppressor that plays roles in CMV accumulation and virulence. The 2b proteins of subgroup IA CMV strains partition between the nucleus and cytoplasm, but the biological significance of this is uncertain. We fused an additional nuclear localization signal (NLS) to the 2b protein of subgroup IA strain Fny-CMV to create 2b-NLS and tested its effects on subcellular distribution, silencing, and virulence. The additional NLS enhanced 2b protein nuclear and nucleolar accumulation, but nuclear and nucleolar enrichment correlated with markedly diminished silencing suppressor activity in patch assays and abolished 2b protein-mediated disruption of microRNA activity in transgenic Arabidopsis. Nucleus/nucleolus-localized 2b protein possesses at least some ability to inhibit antiviral silencing, but this was not sufficient to prevent recovery from disease in younger, developing leaves in Arabidopsis. However, enhanced nuclear and nucleolar accumulation of 2b increased virulence and accelerated symptom appearance in older leaves. Experiments with Arabidopsis lines carrying mutant Dicer-like alleles demonstrated that compromised suppressor activity explained the diminished ability of 2b-NLS to enhance virus accumulation. Remarkably, the increased virulence that 2b-NLS engendered was unrelated to effects on microRNA- or short interfering RNA-regulated host functions. Thus, although nucleus- and nucleolus-localized 2b protein is less efficient at silencing suppression than cytoplasm-localized 2b, it enhances CMV virulence. We propose that partitioning of the 2b protein between the cytoplasmic and nuclear/nucleolar compartments allows CMV to regulate the balance between virus accumulation and damage to the host, presumably to maximize the benefit for the virus. Importance: In this work, the main finding is that nucleus/nucleolus-localized 2b protein is strongly associated with CMV virulence, which is independent of its effect on small RNA pathways. Moreover, this work supports the contention that the silencing suppressor activity of CMV 2b protein is predominantly exerted by that portion of the 2b protein residing in the cytoplasm. Thus, we propose that partitioning of the 2b protein between the cytoplasmic and nuclear/nucleolar compartments allows CMV to regulate the balance between virus accumulation and damage to the host, presumably to maximize the benefit for the virus.
    Full-text · Article · Mar 2014 · Journal of Virology
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