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 pathogenassociated 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.

Antagonistic within‐host interactions between plant viruses: molecular basis and impact on viral and host fitness

“…For a better understanding of possible, although still hypothetical, mechanisms of these phenomena, we highlight briefly the molecular aspects of viral infection and the ensuing plant response. As it is beyond the scope of this article to characterize in detail multi‐layered plant defence strategies, readers are referred to comprehensive reviews on this topic (Coll et al ., ; De Ronde et al ., ; Dodds and Rathjen, ; Ghoshal and Sanfaçon, ; Hou et al ., ; Huot et al ., ; Mandadi and Scholthof, ; Molnar et al ., ; Muthamilarasan and Prasad, ; Pallas and García, ; Pieterse and Van Wees, ).…”

Salicylic Acid Regulates Plasmodesmata Closure during Innate Immune Responses in Arabidopsis

“…For example, plant viruses spread their infectious materials cell to cell (Benitez-Alfonso et al, 2010) through either regulating PD dilation (Waigmann et al, 1994) or modifying PD structure (van Lent et al, 1991;Pouwels et al, 2003,;. Unlike viruses, bacterial pathogens are mostly epiphytic in their lifestyle, and their mode of infection does not require them to move cell to cell (Hou et al, 2009). However, bacterial infection induces the closure of PD, and a loss of PD regulation or a constitutive closure of PD in Arabidopsis thaliana confers either susceptibility or resistance, respectively, to virulent strains of Pseudomonas syringae .…”

An E3 ubiquitin ligase fromNicotiana benthamianatargets the replicase ofBamboo mosaic virusand restricts its replication

“…Plants have evolved various strategies to face rapid environmental changes and pathogen invasions (Boller and Felix, ; Cohn et al ., ). Recognizing and confronting these pathogens are involved in regulating the massive gene expression involved in plant–pathogen interactions (Hou et al ., ). Ubiquitin‐mediated protein degradation is widely used amongst eukaryotes.…”