effectortriggered

Effector-triggered immunity, commonly abbreviated ETI, is a major component of the plant innate immune system. It is activated when plant cells detect specific pathogen-derived molecules known as effectors. Effectors are proteins or other molecules that pathogens deploy to promote infection, and their detection signals that the pathogen is present.

ETI is typically mediated by intracellular immune receptors, often nucleotide-binding leucine-rich repeat proteins (NLRs). These receptors can recognize effectors directly or detect their activity indirectly by monitoring host proteins that the effectors modify. Upon recognition, a robust defense program is initiated, frequently including a hypersensitive response (localized cell death) to contain the pathogen, production of reactive oxygen species, reinforcement of cell walls, and widespread transcriptional changes that activate defense-related genes. Signaling pathways commonly involve hormones such as salicylic acid and, to varying extents, jasmonic acid and ethylene.

ETI is viewed as the second layer of plant innate immunity, following pattern-triggered immunity (PTI). PTI is activated by recognition of conserved microbial features by surface receptors, while ETI typically responds to specific pathogen effectors that have overcome PTI. The interaction between plant R genes and pathogen Avr genes illustrates the gene-for-gene model, underlining an ongoing evolutionary arms race between hosts and pathogens.

While ETI often yields a strong and rapid response, successful pathogens may evolve strategies to suppress or evade recognition. ETI research informs crop improvement, as many resistance (R) genes derived from ETI contribute to durable disease resistance when deployed in crops.