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Fig. 1 | Virology Journal

Fig. 1

From: Regulation of plant antiviral defense genes via host RNA-silencing mechanisms

Fig. 1

"Zig-Zag" model by Jones and Dangl [6] adapted for representing plant defense responses to viruses. Virus-associated molecular patterns, VAMPs, typically double-stranded (ds)RNA of viral origin, can induce either RNAi-based antiviral or a canonical pathogen triggered immunity (PTI) upon recognition by Dicer-like proteins (DCLs) or transmembrane leucine rich pattern-recognition receptors (PRRs), respectively. The PTI response evolves into sequence-specific antiviral silencing and/or into wide-spread suppression of host gene expression. Viruses express virulence effectors (i.e., viral suppressors of RNA silencing, VSRs) that can suppress PTI and lower the level of resistance. In resistant plant accessions, virulence effectors or virus structural components are recognised by intracellular immune receptors, commonly of the NB-LRR type. Immune receptor activation triggers production of reactive oxygen species (ROS), NO, phytohormone signalling (Jasmonate, JA; Ethylene, ET; salicylic acids, SA) and the hypersensitive responses (HR). ETI further induces systemic acquired resistance (SAR)

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