Abstract
In plant−virus interactions, the plant immune system and virulence strategies are under constant pressure for dominance, and the balance of these opposing selection pressures can result in disease or resistance. The naturally evolving plant antiviral immune defense consists of a multilayered perception system represented by pattern recognition receptors (PRR) and resistance (R) proteins similarly to the nonviral pathogen innate defenses. Another layer of antiviral immunity, signaling via a cell surface receptor-like kinase to inhibit host and viral mRNA translation, has been identified as a virulence target of the geminivirus nuclear shuttle protein. The Geminiviridae family comprises broad-host range viruses that cause devastating plant diseases in a large variety of relevant crops and vegetables and hence have evolved a repertoire of immune-suppressing functions. In this review, we discuss the primary layers of the receptor-mediated antiviral immune system, focusing on the mechanisms developed by geminiviruses to overcome plant immunity.
Highlights
The first line of plant defense against pathogens is represented by cell surface-localized pattern recognition receptors (PRRs), which sense and recognize pathogen-associated molecular patterns (PAMPs) presented by the pathogens, or danger-associated molecular patterns (DAMPs), endogenous signals released by the host upon infection [3,4]
These results suggest that PRRs sense viral PAMPs intracellularly, which would require either an endocytic internalization of the PRR sensing extracellular domain or perception via the PRR kinase cytosolic domain
Recent studies have demonstrated that plants deploy both levels of the classic innate immunity, PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI), to fight virus infection, and geminiviruses are not exception
Summary
Successful infection depends on PTI suppression by virulence effectors eliciting effector-triggered susceptibility (ETS) [8,9,10] To overcome these virulence strategies, plant cells have evolved a second line of defense called effector-triggered immunity (ETI), activated in resistant genotypes upon specific interactions between host intracellular receptors (resistance proteins; R) and pathogen avirulence (Avr) effectors [11]. NIK1-mediated antiviral signaling has been shown to suppress global host translation to fight geminiviruses and tobacco rattle virus (TRV) [16,17,18] This minireview focuses on the three layers of receptor-mediated plant antiviral immunity (PTI, ETI, and NIK1-mediated antiviral signaling) and describes the virulence strategies evolved by geminiviruses to overcome these host defense barriers.
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