A holistic view on plant effector-triggered immunity presented as an iceberg model

Area of Science:

• Plant immunity
• Molecular plant-pathogen interactions
• Genetics

Background:

• Plant immunity involves complex, multi-step pathways like pattern-triggered immunity (PTI).
• Pathogens deploy effectors to inhibit PTI, which can trigger effector-triggered immunity (ETI) via plant nucleotide-binding leucine-rich repeat (NLR) receptors.
• A large number of NLRs and effectors exist, yet few are genetically identified as resistance (R) and avirulence (Avr) genes.

Purpose of the Study:

• To propose a model explaining the discrepancy between the large number of plant NLRs/effectors and the limited number of genetically identified R/Avr genes.
• To provide a framework for understanding the dynamics of plant-pathogen molecular interactions.

Main Methods:

• Theoretical modeling based on existing knowledge of plant immunity.
• Analysis of genetic segregation patterns of R and Avr genes.
• Consideration of effector functions and plant susceptibility factors.

Main Results:

• Introduction of the "iceberg model" where most NLR-effector interactions are genetically silent below the surface.
• The model explains the high number of NLRs and effectors by proposing they maintain a silent state.
• The model accounts for reduced virulence upon effector downregulation and the prevalence of lesion-mimic mutants.

Conclusions:

• The "iceberg model" offers a unifying explanation for the genetic invisibility of most plant immune receptors and pathogen effectors.
• The model suggests that many plant susceptibility factors can be targets for pathogen effectors.
• This framework advances our understanding of plant immune system complexity and evolution.