Disease susceptibility in the Zig‐Zag model of host–microbe interactions: only a consequence of immune suppression?

For almost ten years, the Zig-Zag model has provided a convenient framework for explaining the molecular bases of compatibility and incompatibility in plant-microbe interactions (Jones and Dangl, 2006). According to the Zig-Zag model, disease susceptibility is a consequence of the suppression of host immunity during the evolutionary arms race between plants and pathogens. The Zig-Zag model thus fits well with biotrophic interactions, but is less applicable to interactions involving pathogens with a necrotrophic lifestyle. With this opinion piece, we want to persuade readers that the Zig-Zag model might be a versatile tool for explaining most host-pathogen interactions, when it does not consider suppressed immune responses as the only cause for disease susceptibility. We provide examples for the adaptability of the Zig-Zag model to interactions with necrotrophs, after the introduction of a new evolutionary branch. Furthermore, we provide evidence that a more ramified Zig-Zag model can be applied to host-microbe interactions in animal systems. To this end, we compare pro-inflammatory infectious processes in animals with necrotrophic strategies in plants, and suggest that both cumulate in an ETI-derived ramification called “effector-triggered immune pathology” (ETIP)