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

Abstract

Plant resistance (R) proteins perceive specific pathogen effectors from diverse plant pathogens to initiate defense responses, designated effector-triggered immunity (ETI). Plant R proteins are mostly nucleotide binding-leucine rich repeat (NB-LRR) proteins, which recognize pathogen effectors directly or indirectly through sophisticated mechanisms. Upon activation by effector proteins, R proteins elicit robust defense responses, including a rapid burst of reactive oxygen species (ROS), induced biosynthesis and accumulation of salicylic acid (SA), a rapid programmed cell death (PCD) called hypersensitive response (HR) at the infection sites, and increased expression of pathogenesis-related (PR) genes. Initiation of ETI is correlated with a complex network of defense signaling pathways, resulting in defensive cellular responses and large-scale transcriptional reprogramming events. In this review, we highlight important recent advances on the recognition of effectors, regulation and activation of plant R proteins, dynamic intracellular trafficking of R proteins, induction of cell death, and transcriptional reprogramming associated with ETI. Current knowledge gaps and future research directions are also discussed in this review.

Associations with rhizosphere bacteria can confer an adaptive advantage to plants

“…While reminiscent of a defence response, this is distinct from the paradigm of well-characterized defence mechanisms in plants (that is, Resistance ( R ) genes) that achieve specificity at the perception level 41 , but where the inputs from perception of diverse pathogens converge on largely overlapping downstream pathways 42 . Known downstream defence mechanisms are largely blunt force antimicrobial instruments such as plant cell death, reactive oxygen species production, or production of broad-spectrum antimicrobials 43,44 that would not be expected to limit the growth of a narrow group of bacterial taxa. We also did not detect increased expression of defence genes in incompatible accessions; in fact, defence gene induction was more closely correlated with compatibility (Fig.…”

Behind the lines–actions of bacterial type III effector proteins in plant cells

“…This so-called effector-triggered susceptibility is counteracted by a second line of plant defense responses, designated ETI, which is activated by the products of plant resistance ( R ) genes upon detection of individual effector proteins (Wu et al. 2014; Cui, Tsuda and Parker 2015) (Fig. 1A).…”

OsCUL3a Negatively Regulates Cell Death and Immunity by Degrading OsNPR1 in Rice

“…One hallmark of ETI is the hypersensitive response, in which the infection site rapidly undergoes programmed cell death (PCD) that arrests the growth and spread of the pathogen (Wu et al, 2014;Zebell and Dong, 2015). Given its severe consequences for cell fate and its effectiveness in halting pathogen ingress, PCD must be tightly regulated in the absence of pathogen attack (Mukhtar et al, 2016).…”