Suppression of PAMP-triggered immunity (PTI) by effector proteins synthesized by phytopathogens and delivered into cells of infected plant

Abstract

Plant immunity is constituted by multilayered system involving two intertwined lines of defence: a first level of immunity termed PAMP-triggered immunity (PTI) or basal resistance, and a second layer of plant defence, called effector-triggered immunity (ETI). The second line of defence depends on the ability of the plant to recognize phytopathogen-synthesized effector proteins delivered into host plant cells. The effector proteins employ common as well as pathogen-specific strategies to disturb plant immunity and to promote pathogen survival and favor their multiplication. They target pattern-recognition receptors (PRRs) and key components in the PTI signaling pathways, as well as, they interfere with many cellular processes including vesicle transport, cytoskeleton reorganization, proteasome-dependent protein degradation, phytohormone biosynthesis and signaling, and gene expression. This results in effector-triggered susceptibility (ETS). However, in some cases, pathogen effectors are recognized by plant intracellular immune receptors NB-LRR/NLR that identify effector proteins. Conformational changes in the NB-LRR/NLR immune receptors accompanying the recognition of the effector proteins activate intracellular signaling pathways initiating a whole range of defence responses that form the second line of local defence.