Go in for the kill: How plants deploy effector-triggered immunity to combat pathogens. [Corrected].

Area of Science:

• Plant pathology
• Molecular biology
• Immunology

Background:

• Plant resistance (R) proteins mediate effector-triggered immunity (ETI) against pathogens.
• Nucleotide binding-leucine rich repeat (NB-LRR) proteins are key R proteins recognizing pathogen effectors.
• ETI involves complex signaling networks, leading to defense responses like reactive oxygen species (ROS) burst, salicylic acid (SA) accumulation, programmed cell death (PCD), and pathogenesis-related (PR) gene expression.

Purpose of the Study:

• To review recent advances in plant effector-triggered immunity (ETI).
• To discuss effector recognition, R protein regulation, activation, and trafficking.
• To highlight cell death induction and transcriptional reprogramming in ETI, and identify knowledge gaps.

Main Methods:

• Literature review of recent research on plant R proteins and ETI.
• Synthesis of findings on effector recognition mechanisms.
• Analysis of signaling pathways and cellular responses during ETI.

Main Results:

• R proteins, primarily NB-LRRs, recognize pathogen effectors via direct or indirect interactions.
• ETI activation triggers ROS burst, SA accumulation, PCD (hypersensitive response), and PR gene induction.
• ETI involves intricate defense signaling, cellular responses, and transcriptional reprogramming.

Conclusions:

• Recent advances have elucidated key aspects of ETI, including effector recognition and R protein dynamics.
• Understanding ETI is crucial for developing durable crop resistance strategies.
• Further research is needed to address current knowledge gaps in ETI regulation and activation.