The multilevel and dynamic interplay between plant and pathogen

Abstract

Phytopathogens invade into plant apoplast and proliferate by assimilating nutrition from plant cells. Plants depend on sophisticated defensive strategies to resist this invasion. Therefore, pathogenic disease and plant disease resistance are two opposite phases. Fascinating molecular mechanisms uncovered that interactions between plant and pathogen are multilevel and dynamic processes. On one side, plant immunity system contains multiple layers mainly including the perception of common pathogen- associated molecular patterns (PAMPs) using distinct cell-surface pattern-recognition receptors (PRRs) to activate intracellular signaling pathways for broad-spectrum immunity, and the recognition of pathogen virulence proteins by the specific intracellular disease resistance (R) proteins for cultivar-specific immunity. On the opposite side, the bacterial pathogens employ virulence factors, such as phytotoxin and type III effectors (T3SEs) to interfere with the host immunity in different levels. Meanwhile, natural selection drives plants and pathogens to evolve new strategies to confront with each other constantly. The present review highlights recent insights about Arabidopsis immunity and mechanisms for Pseudomonas syringae to counteract this immunity to give a full understanding of plant-pathogen interactions.

Keywords: Pseudomonas syringae; arabidopsis; evolution; plant-pathogen interactions; type III effector.

Figure 1

Interplay between bacterial pathogenesis and plant innate immunity in multiple pathways. Plants recognize PAMPs (flagellin and EF-Tu) through PRRs (FLS2 and EFR) and triggered the first layer of the plant innate immune responses. PRRs trigger the convergent immune signaling including MAP kinase (MAPK) cascade activation and early defense gene transcription controlled by WRKY and other transcription factors. Successful bacterial pathogens have evolved multiple virulence effectors, such as avrPto, avrPtoB, hopAI1, hopF2, hopM1, hopU1, hopI1 and hopT1-1 to suppress PTI and interfere with other resistance pathways. To survive, plants have developed the R proteins to counteract specific avirulence effectors and trigger the ETI. The interactions between type III effectors and intracellular NB-LRR proteins could be direct or indirect through other host proteins.

Figure 2

The balance of regulation between RIN4 and NDR1 in plant immunity. (A) RIN4 suppresses PAMP-induced basal defence; (B) Transgenic Arabidopsis overexpressing RIN4 suppress RPS2-mediated resistance; (C) The cleavage of RIN4 by AvrRpt2 is required for RPS2-mediated resistance; (D) Overexpression of NDR1 hyperactivates AvrRpt2-RPS2 mediated resistance.

Figure 3

Evolution pattern of the type III effectors and their host receptors. (A) N-terminal region of AvrPtoB did as the initial protein to suppress FLS2-medated basal defence, and then Fen was evolved by plant to negate basal defence suppression, and activate defence signaling. To counter recognition by Fen and restore basal defence suppression activity, the N-terminal region of AvrPtoB acquired an E3 ligase domain to mediate the degradation of Fen. Finally, Pto was evolved to be invulnerable to AvrPtoB-mediated ubiquitination and subsequent degradation to restore resistance response. (B) HopAB family type III effectors in Pseudomonas syringae were evolved using the terminal re-assortment.