Antiviral innate immunity in plants.
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Antiviral innate and adaptive immunity mechanisms

This review article summarises the molecular mechanisms of the antiviral immune system in plants and reports the latest breakthroughs relating to plant defence against viruses. Particular attention is given to the immune receptors and transduction pathways in antiviral innate immunity that are involved in pathogen-associated molecular pattern (PAMP)-triggered immunity, effector-triggered immunity and the translational control branch of the NIK1-mediated antiviral signalling, as well as to the adaptive RNA silencing mechanism.

Antiviral innate immunity in plants.
Antiviral innate immunity in plants. (A) PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI) in virus–host interactions. During viral infection, the replication and expression of the viral genome lead to the accumulation of virus-derived nucleic acids with features of pathogen-associated molecular patterns (PAMPs), which may be recognized by host pattern recognition receptors (PRRs) that, in turn, heterooligomerize with co-receptors, such as BAK1 and BKK1, to trigger PTI. Alternatively, PTI may be activated upon PRR recognition of damage-associated molecular patterns (DAMPs), which are induced by infection and delivered to the apoplast by the host cells via the secretory apparatus. In a successful infection, expression of the viral genome results in accumulation of virus effectors to suppress PTI, leading to disease. In resistant genotypes, however, the resistance genes specifically recognize, directly or indirectly, the viral effectors, called avirulence (Avr) factors, activating ETI and conferring resistance. (B) The translational control arm of the NIK1-mediated signalling in antiviral innate immunity. Virus infection-induced oligomerization of NIK1 promotes transphosphorylation at the crucial Thr474, activating the kinase. Alternatively, NIK1 interacts with an unknown ligand-binding LRR-RLK in a stimulus-dependent manner. Although viral infection triggers NIK1-mediated antiviral signalling, the molecular basis of this elicitation is unknown and may be either intracellular virus-derived nucleic acid PAMPs or endogenous DAMPs released in the apoplasts by the host cells. Upon activation, NIK1 indirectly mediates the RPL10 phosphorylation, promoting its translocation to the nucleus, where it interacts with LIMYB to down-regulate the expression of translation-related genes. Therefore, the propagation of the antiviral signal culminates with suppression of host global protein synthesis, which also impairs translation of viral mRNA, as a defence mechanism. In begomovirus–host compatible interactions, the binding of begomovirus NSP to the NIK1 kinase domain (A-loop) inhibits autophosphorylation at Thr474, thereby preventing receptor kinase activation and RPL10 phosphorylation, overcoming this layer of defence. The viral single-stranded DNA replicates via double-stranded DNA intermediates that are transcribed in the nucleus of plant-infected cells. NSP binds to the nascent viral DNA and facilitates its movement to the cytoplasm and acts in concert with the classical movement protein MP to transport the viral DNA to the adjacent, uninfected cells.

Calil and Fontes conclude that plant defence and virulence strategies co-evolve and co-exist; hence, disease development is largely dependent on the extent and rate at which these opposing signals emerge in host and non-host interactions. A deeper understanding of plant antiviral immunity may facilitate innovative biotechnological, genetic and breeding approaches for crop protection and improvement.

This paper is part of the Annals of Botany Special Issue on Plant Immunity. It will be free access till June 2017 and after April 2018.


The Annals of Botany Office is based at the University of Oxford.

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