Effector-triggered defence against apoplastic fungal pathogens

Area of Science:

• Plant pathology
• Molecular plant-microbe interactions
• Plant immunity

Background:

• Existing models of plant immunity, pathogen-associated molecular pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), do not fully explain R gene-mediated resistance to apoplastic fungal pathogens.
• A gap exists in understanding specific resistance mechanisms against foliar fungal pathogens in crops.

Purpose of the Study:

• To propose a new term, 'effector-triggered defence' (ETD), for R gene-mediated resistance against apoplastic fungal pathogens.
• To differentiate ETD from PTI and ETI based on molecular mechanisms and host responses.

Main Methods:

• Conceptual framework development based on existing literature.
• Comparison of molecular components and timing of host cell death in different immunity pathways.

Main Results:

• ETD is mediated by R genes encoding cell surface-localised receptor-like proteins (RLPs) that interact with the receptor-like kinase SOBIR1.
• ETD involves extracellular recognition, contrasting with the intracellular recognition of ETI.
• ETD-associated host cell death is typically delayed compared to the rapid, hypersensitive cell death in ETI.

Conclusions:

• Effector-triggered defence (ETD) provides a more accurate description for a specific type of R gene-mediated resistance.
• Understanding ETD is crucial for developing effective crop protection strategies against fungal diseases.