Zig-Zag Model of Plant Immunity
The Zig-Zag Model is a conceptual framework used to describe the dynamic interaction between plants and pathogens. It illustrates how plants detect and respond to pathogens through their innate immune system, and how pathogens, in turn, evolve to suppress plant immunity. This model was proposed by Jones and Dangl in 2006.
Phase 1: PAMP-Triggered Immunity (PTI)
- PAMPs (Pathogen-Associated Molecular Patterns), also known as MAMPs (Microbe-Associated Molecular Patterns), are conserved microbial molecules (e.g., flagellin, chitin, LPS).
- Recognized by PRRs (Pattern Recognition Receptors) on the plant cell surface.
- This triggers PTI, a broad-spectrum, basal immune response.
Outcome:
Moderate defense response that slows pathogen growth.
2. Phase 2: Effector-Triggered Susceptibility (ETS)
- To overcome PTI, pathogens secrete effectors (virulence proteins) into the host.
- These effectors suppress PTI, leading to ETS, where the plant becomes more susceptible to disease.
Pathogen Strategy:
Inhibits plant defenses and promotes pathogen colonization.
Phase 3: Effector-Triggered Immunity (ETI)
- Plants evolve Resistance (R) proteins (often NB-LRR proteins) that specifically recognize certain effectors (either directly or indirectly).
- This triggers a stronger, faster immune response, called ETI.
- Often includes the Hypersensitive Response (HR)—localized cell death to prevent spread.
Outcome:
Robust defense that halts pathogen growth.
Phase 4: Pathogen Counter-Defense
- Pathogens evolve new effectors or modify existing ones to evade R protein recognition.
- Plants may then evolve new R genes.
Result:
An ongoing evolutionary "arms race", hence the zig-zag pattern.