A model is, essentially, a microcosm of scientific hypothesis generation. At its heart, any model simply acts as a logical machine for deducing conclusions from the restricted set of assumptions that define that model (Gunawardena, 2014). Their purpose is to reduce the complexity of a real-world system to a manageable and understandable level. Models in the scientific sense are abstract representations of reality. Eight years on, we take a fresh look at the model to consider how well it fits its intended purpose, and how a model framework to inspire future researchers in the field of plant–microbe interactions might develop.
The model has captured the imagination of plant pathology researchers and students alike, and has proved to be a powerful conveyor of the principal concepts in plant–pathogen interactions. This branch is called effector-triggered immunity (ETI). The second branch recognizes and responds to virulence factors termed effectors that, in the model, serve to suppress PTI. The first branch recognizes conserved molecules shared by many classes of microbe (pathogen-associated or microbe-associated molecular patterns, PAMPs or MAMPs), and is now called pattern-triggered immunity (PTI). In 2006, Jones and Dangl proposed a simple coevolutionary model of plant–pathogen interactions, called the ‘zigzag’ model, which encompasses two branches of the plant immune system (Jones and Dangl, 2006).
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