A fungal effector hijacks a plastid protein to dampen plant immunity; PR1 is here for rescue.

Abstract

Plants are engaged in a constant battle for survival against pathogens, which triggers a multifaceted immune response characterized by pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) to prevent infection. These two immune responses operate synergistically to enhance plant immunity. PTI is considered the first line of defense involving the recognition of pathogen-associated molecular patterns (PAMPs) by specific receptors in host cells known as pattern recognition receptors (PRRs), which initiate defense signaling. However, many pathogens often overcome the first line of defense (PTI) and successfully deploy effector proteins to promote virulence and subvert plant immunity, leading to host susceptibility. In the counter-defense, the ETI defense mechanism is activated by triggering resistance (R) genes in plants that usually encode nucleotide-binding-leucine-rich-containing (NLR) proteins. During plant-pathogen interactions, transcriptional reprogramming of defense-related genes such as pathogenesis-related proteins and generation of reactive oxygen species (ROS) are essential for facilitating programmed cell death at the infected location to inhibit pathogen proliferation. While ROS and PR protein are critical in plant-pathogen interaction, they are not universally required or effective against all pathogens. Hence, plants' multilayer immune layer is encrypted with the compensatory activation of ETI defense response towards the failure of one component of the defense system to maintain robust immunity.