Abstract
RNA silencing mediated by small RNAs (sRNAs) is a conserved regulatory process with key antiviral and antimicrobial roles in eukaryotes. A widespread counter-defensive strategy of viruses against RNA silencing is to deploy viral suppressors of RNA silencing (VSRs), epitomized by the P19 protein of tombusviruses, which sequesters sRNAs and compromises their downstream action. Here, we provide evidence that specific Nicotiana species are able to sense and, in turn, antagonize the effects of P19 by activating a highly potent immune response that protects tissues against Tomato bushy stunt virus infection. This immunity is salicylate- and ethylene-dependent, and occurs without microscopic cell death, providing an example of “extreme resistance” (ER). We show that the capacity of P19 to bind sRNA, which is mandatory for its VSR function, is also necessary to induce ER, and that effects downstream of P19-sRNA complex formation are the likely determinants of the induced resistance. Accordingly, VSRs unrelated to P19 that also bind sRNA compromise the onset of P19-elicited defense, but do not alter a resistance phenotype conferred by a viral protein without VSR activity. These results show that plants have evolved specific responses against the damages incurred by VSRs to the cellular silencing machinery, a likely necessary step in the never-ending molecular arms race opposing pathogens to their hosts.
Highlights
Plants fight microbial attacks using both constitutive and induced defenses, which include basal and highly specific resistance [1]
This pathogen-associated molecular patterns (PAMPs)-triggered immunity (PTI) may be itself antagonized by adapted pathogens that have evolved virulence effectors to target key PTI components
It has been noted that RNA silencing, a sequence-specific antiviral defense response based on the production of virus-derived 21–24 nt small RNAs on the one hand, and its suppression by virulence effectors, called viral suppressors of RNA silencing (VSRs) on the other, are conceptually similar to PTI
Summary
Plants fight microbial attacks using both constitutive and induced defenses, which include basal and highly specific resistance [1]. PTI (for PAMP-Triggered Immunity), often relies on the detection of highly conserved signature molecules that include fungal polysaccharides or bacterial flagellin, collectively termed pathogen-associated molecular patterns (PAMPs; [1,2]). To circumvent this first layer of defense, many host-adapted microbes produce effector proteins that suppress various steps of PTI [3]. As a counter-response, plants have, in turn, evolved classes of specialized receptors called resistance (R) proteins that directly detect pathogen’s encoded suppressors of PTI, or that sense the molecular consequences of their adverse action on defense-related host factors. The occurrence of HR is classically used to discern PTI from ETI during bacterial or fungal infections [7], an HRindependent process known as Extreme Resistance (ER) is activated by a number of R proteins during ETI against viruses; ER is characterized by the lack of detectable accumulation of the triggering virus, and is accompanied by the onset of a broadspectrum antiviral state in the absence of macroscopic or microscopic cell death lesions [8,9,10,11]
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