Abstract
Plants respond to pathogens using an innate immune system that is broadly divided into PTI (pathogen-associated molecular pattern- or PAMP-triggered immunity) and ETI (effector-triggered immunity). PTI is activated upon perception of PAMPs, conserved motifs derived from pathogens, by surface membrane-anchored pattern recognition receptors (PRRs). To overcome this first line of defense, pathogens release into plant cells effectors that inhibit PTI and activate effector-triggered susceptibility (ETS). Counteracting this virulence strategy, plant cells synthesize intracellular resistance (R) proteins, which specifically recognize pathogen effectors or avirulence (Avr) factors and activate ETI. These coevolving pathogen virulence strategies and plant resistance mechanisms illustrate evolutionary arms race between pathogen and host, which is integrated into the zigzag model of plant innate immunity. Although antiviral immune concepts have been initially excluded from the zigzag model, recent studies have provided several lines of evidence substantiating the notion that plants deploy the innate immune system to fight viruses in a manner similar to that used for non-viral pathogens. First, most R proteins against viruses so far characterized share structural similarity with antibacterial and antifungal R gene products and elicit typical ETI-based immune responses. Second, virus-derived PAMPs may activate PTI-like responses through immune co-receptors of plant PTI. Finally, and even more compelling, a viral Avr factor that triggers ETI in resistant genotypes has recently been shown to act as a suppressor of PTI, integrating plant viruses into the co-evolutionary model of host-pathogen interactions, the zigzag model. In this review, we summarize these important progresses, focusing on the potential significance of antiviral immune receptors and co-receptors in plant antiviral innate immunity. In light of the innate immune system, we also discuss a newly uncovered layer of antiviral defense that is specific to plant DNA viruses and relies on transmembrane receptor-mediated translational suppression for defense.
Highlights
Plants recognize potential pathogens mainly through two classes of distinct immune receptors (Schwessinger and Ronald, 2012; Spoel and Dong, 2012; Zvereva and Pooggin, 2012; Dangl et al, 2013)
In comparison with resistance gene (R gene) against non-viral pathogens, the number of well-studied examples of antiviral R genes is still limited with respect to an understanding of the level of specialization of dominant resistance against viruses and the boundaries of features shared with non-viral effector-triggered immunity (ETI)
Non-self RNA motifs appear to function as PAMPs from RNA viruses, we do not know the identities of virus-derived PAMPs or plant-derived damage-associated molecular patterns (DAMPs) that would induce antiviral PAMP-triggered immunity (PTI)
Summary
Plants recognize potential pathogens mainly through two classes of distinct immune receptors (Schwessinger and Ronald, 2012; Spoel and Dong, 2012; Zvereva and Pooggin, 2012; Dangl et al, 2013). The first class consists of cell-surface associated pattern recognition receptors (PRRs), which are often represented by receptor-like kinases (RLKs) and receptor-like proteins (RLPs; Figure 1)
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