Abstract
Tomato spotted wilt virus (TSWV) is one of the most destructive viral pathogens of plants. Recently, a single dominant gene conferring complete resistance to TSWV (RTSW) was identified in Nicotina alata and introgressed into cultivated tobacco (N. tabacum). However, whether the TSWV carries an avirulence (Avr) factor directed against RTSW remains obscure. In the present study, we identified the non-structural protein (NSm), the movement protein of TSWV, which is an RTSW-specific Avr factor, by using two different transient expression systems. Using amino acid (aa) substitution mutants, we demonstrated the ability to induce RTSW-mediated hypersensitive response (HR) of NSm is independent of its movement function. Moreover, key substitutions (C118Y and T120N), a 21-aa viral effector epitope, and different truncated versions of NSm, which are responsible for the recognition of the Sw-5b resistance gene of tomato, were tested for their ability to trigger HR to TSWV in tobacco. Together, our results demonstrated that RTSW-mediated resistance is triggered by NSm in the same way as by Sw-5b, however, via different elicitor active sites. Finally, an Avr gene-based diagnostic approach was established and used to determine the presence and effectiveness of resistance genes in tobacco.
Highlights
According to the zigzag model of plant–microbe interactions [1], the plant’s innate immune system is broadly divided into two different layers: pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI)
We show that the NSm protein of Tomato spotted wilt virus (TSWV) acts as the Avr determinant of resistance to TSWV (RTSW)-based resistance using two different transient expression systems
The results showed that both HSR203J and pathogenesis-related 1 (PR1) genes were and dramatically up-regulated in N. alata, Polalta, and K326RTSW leaves inoculated with TSWV compared with mock-inoculated leaves or TSWV-inoculated leaves of N. benthamiana, K326 and K326rtsw, all of which showed low levels of expression of HSR203J and PR1 genes (Figure 1D)
Summary
According to the zigzag model of plant–microbe interactions [1], the plant’s innate immune system is broadly divided into two different layers: pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI). PAMPs, such as bacterial flagellin and fungal chitin, and the corresponding membrane-anchored pattern recognition receptors (PRRs) of plants, which serve as the first line of defense against invading pathogens. To counteract ETS, plants have evolved intracellular resistance (R) proteins, which directly or indirectly recognize pathogen effectors or avirulence (Avr) factors and activate ETI, which is often manifested in the form of a hypersensitive. More and more R proteins and Avr factors characterized in different viruses substantiate the notion that plants deploy the innate immune system to fight viruses in a typical ETI-based manner [4]
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