Effector-Triggered Immunity: From Pathogen Perception to Robust Defense

Abstract

In plant innate immunity, individual cells have the capacity to sense and respond to pathogen attack. Intracellular recognition mechanisms have evolved to intercept perturbations by pathogen virulence factors (effectors) early in host infection and convert it to rapid defense. One key to resistance success is a polymorphic family of intracellular nucleotide-binding/leucine-rich-repeat (NLR) receptors that detect effector interference in different parts of the cell. Effector-activated NLRs connect, in various ways, to a conserved basal resistance network in order to transcriptionally boost defense programs. Effector-triggered immunity displays remarkable robustness against pathogen disturbance, in part by employing compensatory mechanisms within the defense network. Also, the mobility of some NLRs and coordination of resistance pathways across cell compartments provides flexibility to fine-tune immune outputs. Furthermore, a number of NLRs function close to the nuclear chromatin by balancing actions of defense-repressing and defense-activating transcription factors to program cells dynamically for effective disease resistance.

TIR-only protein RBA1 recognizes a pathogen effector to regulate cell death inArabidopsis

“…NLRs can detect pathogen effectors either directly, as nominal ligands, or indirectly, via the activity of an effector on a host target or the decoy of a target (35). To test whether RBA1 directly or indirectly sensed HopBA1, we assayed for physical interactions between the two proteins.…”

On plant defense signaling networks and early land plant evolution

“…The pathogen recognition system is based upon two components: pattern triggered immunity (PTI) and effector triggered immunity (ETI) [6]. The latter is more specific towards the infecting pathogen because plant resistance genes ( R genes) recognize effector proteins secreted by, and specific to, a certain pathogen [51]. PTI causes, for example, stomata closure and cell wall reinforcements at the site of pathogen attack (e.g., through callose deposition, formation of papillae [deposits consisting of callose, phenolic compounds and polysaccharides], and lignification) [52-55].…”

“…PTI can also result in cell death caused by the release of reactive oxygen species (ROS) [56]. Additionally, ROS production and thus the initiation of the hypersensitive response (HR) is a classical hallmark of R gene-based immunity [51]. …”

“…ETI requires the presence of R proteins to detect pathogen secreted effector proteins either through direct binding or by monitoring whether other host proteins are altered by the actions of effectors [51]; such alterations can include changes in protein conformation and/or phosphorylation status [82,83]. Once R proteins detect an effector protein of a pathogen, they induce pathogen-specific immune responses [84-86].…”

Plasma Membrane Microdomains Are Essential for Rac1-RbohB/H-Mediated Immunity in Rice

“…This immune system is termed MAMPtriggered immunity (MTI) and leads to the generation of reactive oxygen species (ROS), calcium influx, and biosynthesis of phytoalexins (Boller and Felix, 2009). The second layer is effectortriggered immunity (ETI), which is induced by the perception of pathogen effectors by resistance (R) proteins (Cui et al, 2015). In both immune systems, the plasma membrane (PM) is important because it is the first point of contact between plant cells and pathogens.…”