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. 2012 Oct 29;4(11):2578–2597. doi: 10.3390/v4112578

Figure 1.

Figure 1

Zig-zag model for evolution of innate immunity- and silencing-based plant defense against viral and non-viral pathogens (adopted and extended from Jones and Dangl 2006 [10]). The ultimate amplitude of disease resistance or susceptibility is proportional to [PTI + Silencing – ETS + ETI]. In phase 1, plants detect pathogen-associated molecular patterns (PAMPs) and host danger-associated molecular patterns (DAMPs) via pattern-recognition receptors (PRRs) to induce pattern-triggered immunity (PTI) and, in the case of viral pathogens, plants additionally detect viral double-stranded RNA (dsRNA) to trigger RNA silencing. In phase 2, successful viral and non-viral pathogens deliver effectors/suppressors that interfere with both PTI and silencing, resulting in effector-triggered susceptibility (ETS). In phase 3, one effector or suppressor is recognized directly or indirectly by an NB-LRR protein, activating effector-triggered immunity (ETI), an amplified version of PTI that often passes a threshold for induction of hypersensitive response (HR) and programmed cell death (PCD). In phase 4, pathogen isolates are selected that have lost or modified the specifically recognized effector/suppressor, and perhaps gained a new effector that can help the pathogen to suppress ETI. A new plant NB-LRR allele is then evolved and selected that can recognize the newly acquired effector, resulting again in ETI.